Scald Group Research Articles

77 A Comparison of Large Tbsa Scald Versus Flame Burns in Young Children

Abstract Introduction It is generally accepted that children with large total body surface area (TBSA) flame burns have worse outcomes as compared to those with scald injury. Anecdotally, we have observed the opposite. We sought to compare outcomes of patients using data from the Pediatric Injury Quality Improvement Collaborative (PIQIC). Methods This multicenter, retrospective cohort study collected data from 4 pediatric hospitals participating in PIQIC over a 10 year period. Exclusion criteria were TBSA <15% and mechanism not scald or flame. Patients were categorized by age in years: 0 to <3, toddler; 3 to <10, child; and age ≥ 10. Demographics, clinical features, and adverse events were collected. Models were controlled for percent full thickness burn. Results Due to small sample size of age >10, this group was excluded. 164 patients were identified: 96 (59%) with scald and 68 (41%) were flame. Patients in the toddler group were mainly scalds (N=73, 58%) while the child group was mostly flame (N=52, 67%). Only 28% of scald patients had full-thickness burns compared to 67% of flames. In the scald group, toddlers experienced significantly longer PICU LOS and mechanical ventilator (MV) days than the child group (13 vs. 5 MV days, p < 0.001). Hospital LOS was significantly higher in the child group compared to toddlers. There was trend of higher incidence of sepsis, nosocomial infection, and abdominal catastrophe in toddlers. All mortalities were observed in the child group. In flame patients, toddlers had no mortalities, cases of sepsis or abdominal catastrophe. Toddlers had significantly shorter hospital LOS (18 vs 25, p< 0.001), PICU LOS (9 [1-14] vs 7 [2-18], p< 0.001), and MV days (6 vs. 9, p< 0.001). Older patients with flame burns had higher %TBSA and full-thickness burns. Odds of mortality in both mechanisms was significantly increased for higher TBSA. Each 1% increase in TBSA related to an average 3% increase mortality (OR=1.03, 95% CI: (1.00, 1.06), P=0.04). Separating mechanisms, the model determined mortality was affected by age. While scalds had significantly reduced mortality (OR=0.05, 95% CI: (0.00, 0.057), P=0.02), each additional year of age increased mortality by 42% (OR=1.42, 95% CI: (1.07, 1.89), P=0.02). Each additional year of age resulted in an 18% reduction in nosocomial infection (OR=0.83 95% CI: (0.73,0.96), P=0.01). Conclusions Given the differences in hospital and PICU LOS, MV days, and complication rates, this study confirms that not all burns carry the same risks across age groups and mechanisms. Despite lower rates of full thickness burns, younger patients with scalds may have a longer PICU course, more time on the ventilator, and increased risk of sepsis, nosocomial infection, and abdominal catastrophe than similarly aged patients with flame burns or older patients with scalds. Applicability of Research to Practice Burn mechanism and patient age should be considered in addition to TBSA and burn thickness when caring for a critically ill patient.

Murine scald models characterize the role of neutrophils and neutrophil extracellular traps in severe burns.

Severe burns cause unique pathophysiological alterations especially on the immune system. A murine scald model was optimized as a basis for the understanding of immunological reactions in response to heat induced injury. The understanding of the roles of neutrophil extracellular traps (NETs) and DNases will support the development of new surgical or pharmacological strategies for the therapy of severe burns. We studied C57BL/6 mice (n=30) and employed four scalding protocols with varying exposure times to hot water. An additional scald group with a shorter observational time was generated to reduce mortality and study the very early phase of pathophysiology. At 24h or 72h, blood was drawn and tissue (wound, liver, lung, spleen) was analyzed for the presence of NETs, oxidative stress, apoptosis, bacterial translocation, and extracellular matrix re-organization. In addition, we analyzed the transcriptome from lung and liver tissues. Exposure to hot water for 7s led to significant systemic and local effects and caused considerable late mortality. Therefore, we used an observation time of 24h in this groups. To study later phases of burns (72h) an exposure time of 6s is optimal. Both conditions led to significant disorganization of collagen, increased oxidative stress, NET formation (by immunodetection of H3cit, NE, MPO), apoptosis (cC3) and alterations of the levels of DNase1 and DNase1L3. Transcriptome analysis revealed remarkable alterations in genes involved in acute phase signaling, cell cohesion, extracellular matrix organization, and immune response. We identified two scald models that allow the analysis of early (24h) or late (72h) severe burn effects, thereby generating reproducible and standardized scald injuries. The study elucidated the important involvement of neutrophil activity and the role of NETs in burns. Extensive transcriptome analysis characterized the acute phase and tissue remodeling pathways involved in the process of healing and may serve as crucial basis for future in-depth studies.

Effects and mechanism of diammonium glycyrrhizinate on liver injury in severely scalded rats

Objective: To investigate the effects and mechanism of diammonium glycyrrhizinate (DG) on liver injury in severely scalded rats. Methods: The experimental research method was used. Fifty-four female Sprague-Dawley rats aged 7-9 weeks were divided into sham injury group with simulated injury on the back, and simple scald group and scald+DG group with scald of 30% total body surface area on the back, with 18 rats in each group. Rats in sham injury group were not specially treated after injury, and rats in simple scald group and scald+DG group were rehydrated for antishock. Besides, rats in scald+DG group were injected intraperitoneally with 50 mg/kg DG at post injury hour (PIH) 1, 25, and 49. Rats in the three groups were collected, the serum content of liver function injury related indexes including aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), total protein, and albumin was measured by automatic biochemical assay analyzer, and serum content of ornithine carbamoyl transferase (OCT) was measured by enzyme-linked immunosorbent assay method at PIH 24, 48, and 72; hepatic histopathological changes at PIH 72 were observed by hematoxylin-eosin staining; the mRNA expressions of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), glucose regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), and protein kinase R-like endoplasmic reticulum kinase (PERK) in liver tissue were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction at PIH 24, 48, and 72. The protein expressions of Bcl-2, Bax, GRP78, PERK, and ATF4 in liver tissue were detected by Western blotting at PIH 72 in sham injury group and PIH 24, 48, and 72 in simple scald group and scald+DG group. The number of samples was 6 in each group at each time point. Data were statistically analyzed with analysis of variance for factorial design, one-way analysis of variance, and Bonferroni test. Results: Compared with that in sham injury group, the serum content of AST, ALT, and LDH was significantly increased (P<0.01), and the serum content of total protein and albumin was significantly decreased (P<0.05 or P<0.01) of rats in simple scald group at all post-injury time points. Compared with those in simple scald group, the serum AST content of rats in scald+DG group at PIH 24 was decreased significantly (P<0.05); the serum AST, ALT, and LDH content of rats in scald+DG group at PIH 48 was decreased significantly (P<0.01), and the serum total protein content was increased significantly (P<0.01); the serum AST, ALT, and LDH content of rats in scald+DG group at PIH 72 was decreased significantly (P<0.01), and the serum total protein and albumin content was increased significantly (P<0.01). At PIH 24, 48, and 72, the serum OCT content of rats in simple scald group was (48.5±3.9), (40.8±2.4), and (38.7±2.0) U/L, which was significantly higher than (15.1±2.5), (15.7±2.6), and (16.4±3.7) U/L in sham injury group (P<0.01), and (39.0±4.5), (31.8±2.0), and (22.1±2.6) U/L in scald+DG group (P<0.05 or P<0.01). At PIH 72, the cells in liver tissue of rats in sham injury group had normal morphology and regular arrangement, with no obvious inflammatory cell infiltration; the cells in liver tissue of rats in simple scald group had disordered arrangement, diffuse steatosis, and moderate inflammatory cell infiltration; the cells in liver tissue of rats in scald+DG group arranged regularly, with scattered steatosis and a small amount of inflammatory cell infiltration. Compared with those in sham injury group, the Bcl-2 mRNA (P<0.05 or P<0.01) and protein expressions of liver tissue were significantly decreased, and the mRNA (P<0.01) and protein expressions of Bax were significantly increased in rats in simple scald group at PIH 24, 48, and 72. Compared with those in simple scald group, the mRNA (P<0.05) and protein expressions of Bax in liver tissue of rats in scald+DG group were decreased significantly at PIH 48; the mRNA (P<0.01) and protein expressions of Bax in liver tissue of rats in scald+DG group were significantly decreased, and the mRNA (P<0.01) and protein expressions of Bcl-2 were significantly increased at PIH 72. Compared with those in sham injury group, the mRNA (P<0.05 or P<0.01) and protein expressions of ATF4, GRP78, and PERK in liver tissue were significantly increased in rats in simple scald group at all post-injury time points. Compared with those in simple scald group, the mRNA (P<0.01) and protein expressions of ATF4 in liver tissue of rats in scald+DG group at PIH 48 were significantly decreased, and the mRNA (P<0.05 or P<0.01) and protein expressions of ATF4, GRP78, and PERK were significantly decreased in liver tissue of rats in scald+DG group at PIH 72. Conclusions: DG can effectively reduce the degree of liver injury in rats after severe scald, and the mechanism may involve alleviating endoplasmic reticulum stress and mitigating mitochondrial damage.

Comparison of Work- and Nonwork-Related Lower Extremity Burn Injuries: A Retrospective Analysis.

Lower extremity burn injuries are among the most affected anatomical regions in hospitalized burn patients. Our objective was to compare burn patients with work-related isolated lower extremity burn injuries (w-ILEBI) and patients with nonwork-related isolated lower extremity burn injuries (nw-ILEBI). Sixty-four (15.7%) of 407 patients (16-92 years) were in the w-ILEBI cohort. The most extensive burn wounds were among patients in the fire-flame group with a median total body surface area percent (%TBSA) of 27.0 (interquartile range = 11.0%-45.0%). While 50 (76.9%) patients in the electrical group had full-thickness burns, 99 (60%) of the cases in the scald group had superficial partial-thickness burns. Blood and wound sample cultures were positive in 42 (29.4%) patients in the fire-flame group. Approximately one-third of patients in the fire-flame/electrical group required escharotomy/fasciotomy procedures, only one (0.6%) case in the scald group, and none in the chemical/contact groups. Thirty-three (51%) of the patients in the electrical group underwent skin grafting, but 14 (21.5%) required amputations. The highest mortality was detected in 27 (18.9%) patients in the fire-flame group. This study revealed several differences in clinical characteristics of isolated lower extremity burn injuries (ILEBI): burn mechanism and depth, total body surface area percent (%TBSA), infection, surgery requirements, laterality, and mortality. Within the scope of occupational health and safety measures, protective clothing and increased workplace and safety training for employers/employees should be implemented.

Lytic cocktail: An effective method to alleviate severe burn induced hyper-metabolism through regulating white adipose tissue browning

BackgroundBrowning of white adipose tissue is associated with elevated resting metabolic rates and is considered to be one of the indispensable causes of hypermetabolism in burn patients. Hypermetabolism means increased resting energy expenditure, raised body temperature and acute-phase proteins. Persistently elevated levels of circulating stress hormones have been reported to induce browning of subcutaneous white adipose tissue. The lytic cocktail is a combination of medicines pethidine, chlorpromazine, and promethazine that has been used clinically in sedation for the management of patients. As reported this sedative treatment can reduce the expression of catecholamines in major burn rats. Thus, in this paper we focused on the effects of lytic cocktail in the regulation of white adipose tissue browning and hypermetabolism and we further investigated the underlying mechanism. MethodsA 30% total body surface area (TBSA) Ⅲ degree scald rat model was used for this study. The rats were randomly divided into a sham scald group, a scalding with immediate resuscitation group, and a group of scalding with immediate resuscitation and lytic cocktail treatment. The levels of norepinephrine and epinephrine in plasma were dynamically detected. Changes of the rat body weight and food intake were recorded and compared as indexes of metabolism responses after post-scalding. For the study of white adipose tissue browning, inguinal adipose tissue was used. Metabolic changes, while indicatives of white fat browning were measured by PET/CT. The expression of white adipose browning related proteins and the changes of mitochondria number were used to assess browning of inguinal adipose. ResultsThe level of plasma catecholamines norepinephrine and epinephrine in the lytic cocktail-treated group was significantly lower than the other two groups. Morphology and PET/CT showed that the inguinal white adipose browning was inhibited in the lytic cocktail treated group, whereas scalding with immediate resuscitation group showed browning of white adipose. The number of mitochondria, the expressions of white adipose browning related proteins in the lytic cocktail group were also significantly lower than that of the group of scalding with immediate resuscitation. ConclusionBy reducing expression of heat-related proteins, the application of lytic cocktail medicines inhibits the white adipose tissue browning, which suppresses hypermetabolism in scalded rats. The mechanism might be related to decreased expression levels of stress hormones induced by lytic cocktail. This research suggests that lytic cocktails may be an effective treatment for hypermetabolism after severe burn injury.

Roles of adenosine monophosphate activated protein kinase in skeletal muscle atrophy in rats with severe scald

Objective: To investigate the expression and phosphorylation level change of adenosine monophosphate activated protein kinase (AMPK) in skeletal muscle of severely scald rats and its roles in skeletal muscle atrophy in severely scalded rats. Methods: The experimental research method was applied. Totally 100 6-week-old male Wistar rats were divided into sham injury group and scald group according to the random number table, with 50 rats in each group. After weighing the body weight, rats in scald group were inflicted with full-thickness scald of 30% total body surface area on the back, and rats in sham injury group were simulated with scald. At 6 h and on 1, 3, 5, and 7 d post injury, 10 rats in each group were taken to measure their body weights and weights of extensor digitorum longus and soleus muscle. At 6 h and on 1, 3, 5, and 7 d post injury, the tibialis anterior muscles were collected, the mRNA expressions of muscle atrophy F-box protein (MAFbx) and muscle-specific RING finger protein 1 (MuRF1) were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction; the content of adenosine monophosphate (AMP), adenosine diphosphate, and adenosine triphosphate (ATP) were detected by high performance liquid chromatography, and AMP/ATP ratio and energy charge were calculated; the protein expressions of AMPK-α and phosphorylated AMPK-α (p-AMPK-α) were detected by Western blotting, and the p-AMPK-α/AMPK-α ratio was calculated, with sample number of 4 in each time point of each group. Data were statistically analyzed with analysis of variance for factorial design and least significant difference test. Results: The body weights of rats in 2 groups before injury and at each time point post injury were close (P>0.05). At 6 h post injury, the weight of extensor digitorum longus of rats in scald group was (0.107±0.007) g, which was significantly heavier than (0.086±0.0607) g of sham injury group (P<0.01). On 3 d post injury, the weight of extensor digitorum longus of rats in scald group was (0.083±0.016) g, which was significantly lighter than (0.102±0.005) g of sham injury group (P<0.01). The weight of soleus of rats in 2 groups were close at each time point post injury (P>0.05). Compared with those of sham injury group, the mRNA expression of MAFbx in tibialis anterior muscle of rats in scald group was significantly up-regulated at 6 h post injury (P<0.01), and the mRNA expressions of MuRF1 in tibial anterior muscle of rats in scald group were significantly up-regulated at 6 h and on 1 d post injury (P<0.01). At 6 h and on 7 d post injury, compared with those of false injury group, the AMP/ATP ratios of the tibial anterior muscle of rats in scald group were significantly increased (P<0.05 or P<0.01), and energy charges of the tibial anterior muscle of rats in scald group were significantly decreased (P<0.01). At each time point post injury, the protein expressions of AMPK-α of the tibial anterior muscle of rats in 2 groups were close (P>0.05). The p-AMPK-α/AMPK-α ratios of the tibial anterior muscle of rats in scald group at 6 h and on 7 d post injury were significantly higher than those in sham injury group (P<0.05 or P<0.01). Conclusions: The decrease in energy charge and increase in AMP/ATP ratio of skeletal muscle of rats after severe scald activate AMPK. The activation of AMPK in the early stage of injury is consistent with the up-regulation of MAFbx and MuRF1 expressions and down-regulation of skeletal muscle weight. The above-mentioned changes may be one of the molecular mechanisms of skeletal muscle atrophy in rats with severe scald.

BFGF ameliorates intestinal mucosal permeability and barrier function through tight junction proteins in burn injury rats

BackgroudTo investigate the protective effect of exogenous basic fibroblast growth factor (bFGF) treatment on the intestinal mucosa in scalded rats. MethodsThirty-six SD rats were randomly divided into 3 groups (n = 12): sham group, scald group and bFGF group (0.5 mg/kg). Intestinal barrier dysfunction was evaluated by permeability of intestinal mucosa to fluorescein isothiocyanate (FITC)-dextran and Chiu’s grading system. H&E staining was used to detect the morphological changes of intestinal mucosa. Immunohistochemistry was used to observe zonula occludens-1 (ZO-1) and occludin. Western blot assay was used to detect the expression of ZO-1, Claudin-1, occludin and myosin light-chain kinase (MLCK). ResultsThe results demonstrated that following bFGF treatment, permeability of the intestinal epithelium barrier of was significantly decreased compared to scald group. H&E staining and Chiu’s grading were consistent with previous result. The expression of ZO-1, Claudin-1, occludin in bFGF group were significantly increased compared to scald group, while MLCK protein was decreased. ConclusionsbFGF ameliorates permeability of intestinal mucosa after burns. The possible mechanism may be relate to bFGF could increase the expression level of tight junction proteins (TJPs).

Effect of alprostadil in early wound healing of rats with deep partial-thickness scald

Objective: To explore the effect of alprostadil in early wound healing of rats with deep partial-thickness scald. Methods: Ninety specific pathogen free healthy Sprague-Dawley rats (half males and half females) were divided into sham scald group, simple scald group, and alprostadil group using the random number table with 30 rats in each group. Rats in sham scald group were sham injured, and rats in the other 2 groups were inflicted with deep partial-thickness scald of 30% total body surface area on the back. Immediately after scald, rats in the 3 groups received anti-shock treatment. Two hours post scald, rats in sham scald group and simple scald group were injected intraperitoneally with 1 mL normal saline, and rats in alprostadil group were injected intraperitoneally with 1 mL alprostadil injection, once a day and continued for 14 days. On post scald day (PSD) 3, 7, and 14, 10 rats in each group were collected for observing the general wound conditions and the wound healing rates of rats in 2 scald groups were calculated, abdominal aortic blood of 2 mL from each rat were collected to detect serum thromboxane B2 by enzyme-linked immunosorbent assay, and wound tissue on the back was collected to examine pathomorphological change by hematoxylin-eosin staining and to detect wound microvessel density (MVD) by immunohistochemical staining. Data were statistically analyzed with analysis of variance of factorial design, t test, Kruskal-Wallis H test, Mann-Whitney U test, and Bonferroni correction. Results: (1) There was no scald wound in rats in sham scald group. On PSD 3, wounds of rats in simple scald group and alprostadil group formed dry eschar. On PSD 7 and 14, wound areas of rats in alprostadil group were significantly smaller than those of rats in simple scald group, and with less exudation. (2) On PSD 3, the wound healing rates of rats in simple scald group and alprostadil group were similar (t=1.167, P>0.05). On PSD 7 and 14, the wound healing rates of rats in alprostadil group were significantly higher than those in simple scald group (t=8.657, 33.050, P<0.01). (3) On PSD 3, 7, and 14, the levels of serum thromboxane B2 of rats in simple scald group and alprostadil group were (541±22), (607±47), (688±21), (326±25), (271±21), (135±27) pg/mL, significantly higher than (17±6), (16±4), (16±4) pg/mL of rats in sham scald group (t=72.977, 39.685, 102.076, 37.033, 37.253, 13.845, P<0.01). On PSD 3, 7, and 14, the levels of serum thromboxane B2 of rats in alprostadil group were significantly lower than those in simple scald group (t=20.637, 20.651, 51.680, P<0.01). (4) Normal epidermis and dermis were seen in rats in sham scald group. On PSD 3, a large number of necrotic tissue and inflammatory cells infiltration were seen in wounds of rats in simple scald group, while a little new epithelium formation and some inflammatory cells infiltration were seen in wounds of rats in alprostadil group. On PSD 7 and 14, the new epithelium of rats in alprostadil group was significantly thicker than that in simple scald group, and epidermis formed gradually in alprostadil group. (5) On PSD 3, 7, and 14, the wound MVD of rats in simple scald group and alprostadil group were significantly higher than those in sham scald group (Z=-3.780, -3.781, -3.780, -3.780, -3.781, -3.780, P<0.01). On PSD 3, the wound MVD of rats in simple scald group and alprostadil group were similar (Z=-1.965, P>0.05). On PSD 7 and 14, the wound MVD of rats in alprostadil group were significantly higher than those in simple scald group (Z=-3.780, -3.780, P<0.01). Conclusions: The early intervention with alprostadil can significantly improve microcirculation of deep partial-thickness scald wound, reduce inflammatory cell infiltration, promote the formation of new blood vessels, thus promoting wound healing.

Effects of sodium butyrate on intestinal barrier of severe scald mice and the related mechanism

Objective: To investigate the effects of sodium butyrate on intestinal barrier of the severe scald mice and the related mechanism. Methods: Eighteen C57BL/6 female mice, aged eight to twelve weeks, were divided into sham scald group, pure scald group, and scald+ sodium butyrate group according to random number table, with 6 mice in each group. Back of each mouse in pure scald group and scald+ sodium butyrate group were immersed into 90 ℃ water for 9 s, causing full-thickness scald of 30% total body surface area, while back of each mouse in sham scald group were immersed into 37 ℃ water for 9 s, causing sham injury. All of the mice in 3 groups were intraperitoneally injected with 1 mL sterile lactated Ringer's solution immediately after injury. Besides, mice in scald+ sodium butyrate group were intraperitoneally injected with 300 mg/kg sodium butyrate at 30 min before injury and immediately after injury, while mice in sham scald group and pure scald group were intraperitoneally injected with the same volume of sterile phosphate buffer solution. At post injury hour (PIH) 24, portal vein of mice in 3 groups was harvested, intestinal permeability was measured by fluorescin isothiocyanate-dextran fluorescence probe tracing method, then lileal tissue of mice in 3 groups was harvested, protein expressions of zonula occludens l (ZO-1), occludin, claudin-1, claudin-2, nucleotide-binding oligomerization domain-containing protein-like receptor family pyrin domain containing 3 (NLRP3), interleukin-1β (IL-1β), and IL-18 were detected by Western blotting, and distribution of ZO-1 in intestinal mucosa was observed by indirect immunofluorescence. Data were processed with one-way analysis of variance, least-significant difference test, and Bonferroni correction. Results: (1) At PIH 24, the intestinal permeability of mice in sham scald group, pure scald group, and scald+ sodium butyrate group was 0.88±0.19, 2.62±0.48, 1.23±0.16, respectively. Compared with that in sham scald group, the intestinal permeability of mice in pure scald group was significantly elevated (P<0.01), while the intestinal permeability of mice in scald+ sodium butyrate group showed no obvious change (P>0.05). Compared with that in pure scald group, the intestinal permeability of mice in scald+ sodium butyrate group was significantly decreased (P<0.01). (2) At PIH 24, compared with those in sham scald group, the protein expressions of ZO-1, occludin, and claudin-1 of mice in pure scald group and scald+ sodium butyrate group were significantly decreased (P<0.05), while the protein expression of claudin-2 was significantly increased (P<0.05). At PIH 24, compared with those of pure scald group, the protein expressions of ZO-1 and occludin of mice in scald+ sodium butyrate group were significantly elevated (P<0.05), while the protein expression of claudin-2 was significantly decreased (P<0.05), the protein expression of claudin-1 showed no significant difference (P>0.05). (3) At PIH 24, compared with those in sham scald group, the protein expressions of NLRP3, IL-1β, and IL-18 of mice in pure scald group and scald+ sodium butyrate group were significantly increased (P<0.05). Compared with those of pure scald group, the protein expressions of NLRP3, IL-1β, and IL-18 of mice in scald+ sodium butyrate group were significantly decreased (P<0.05). (4) At PIH 24, ZO-1 in intestinal mucosa of mice in sham scald group was distributed smoothly, continuously and homogeneously along the membrane. ZO-1 in intestinal mucosa of mice in pure scald group was distributed unsmoothly with breaks. The distribution of ZO-1 in intestinal mucosa of mice in scald+ sodium butyrate group was ameliorated compared with that in pure scald group. Conclusions: Sodium butyrate can inhibit the activation of NLRP3 inflammasome and decrease the production of IL-1β and IL-18 in intestinal mucosa of severe scald mice, which protects the intestinal barrier function by alleviating the alteration of tight junction protein expression and localization.

Significance of intestinal fatty acid binding protein in evaluation of intestinal barrier dysfunction of mice at early stage of severe burn injury

Objective: To investigate the significance of intestinal fatty acid binding protein (IFABP) in the evaluation of intestinal barrier dysfunction of mice at the early stage of severe burn injury. Methods: Thirty-six 8-week-old C57BL/6 male mice were collected and divided into normal control group (n=6) and scald group (n=30) according to random number table. Back of each mouse in scald group was placed into hot water of 90 ℃ for 10 s, causing full-thickness scald (hereinafter refer to as burn) of 30% total body surface area, while mice in normal control group were not inflicted with burns. Six mice in normal control group were taken, and 6 mice in scald group at 1, 2, 6, 12, and 24 h post injury were taken respectively. The portal vein blood of each mouse was extracted and the plasma was separated to measure intestinal permeability with fluorescin isothiocyanate-dextran fluorescence probe tracing method and plasma IFABP content by enzyme-linked immunosorbent assay. The distal ileum tissue of mice in normal control group and scald group at each time point post injury was collected to observe the morphology of the intestinal mucosa tissue by hematoxylin-eosin staining. Data were processed with one-way analysis of variance and Student-Newman-Keuls test, and pearson correlation test was used to analyze the correlation between intestinal permeability and plasma IFABP content of burned mice. Results: (1) At 1, 2, 6, 12, and 24 h post injury, the intestinal permeability of mice in scald group was 2.7±0.8, 5.4±2.5, 7.3±4.2, 12.4±6.1, 1.4±0.7, respectively, obviously higher than 1.0±0.4 of normal control group (P<0.05 or P<0.01). The intestinal permeability of mice in scald group showed an increasing trend post injury, reaching the peak at 12 h post injury, and rapidly falling back at 24 h post injury. (2) At 1, 2, 6, 12, and 24 h post injury, the plasma IFABP content of mice in scald group was (64±11), (59±12), (76±18), (111±22), and (66±10) ng/mL, obviously higher than (35±8) ng/mL in normal control group (P<0.05 or P<0.01). The plasma IFABP content of mice in scald group showed an increasing trend post injury, reaching the peak at 12 h post injury, and rapidly decreasing at 24 h post injury. (3) Uniform thickness of mucosa, intact epithelia, regularly arranged villi, and no inflammatory cell infiltration were observed in ileum of mice in normal control group. In ileum of mice in scald group, shortened villi of mucosa with different degrees, edema of lamina propria, and infiltration of neutrophils were observed at 1 and 2 h post injury; obviously damaged and partially exfoliated ileal mucosa, disorderly arranged and broken villi, degenerated and necrotic epithelial cells, dilated central lacteal, and infiltration of lymphocytes and neutrophils were observed at 6 and 12 h post injury; the damage of ileal mucosa was alleviated, and basically intact epithelia, dilated central lacteal, and infiltration of inflammatory cells were observed at 24 h post injury. (4) There was a significantly positive correlation between the intestinal permeability and the plasma IFABP content of burned mice (r=0.841, P<0.05). Conclusions: The plasma IFABP can be used as a good biological indicator for the evaluation of intestinal barrier dysfunction of mice at the early stage of severe burn injury.

Effects of insulin therapy on skeletal muscle wasting in severely scalded rats and its related mechanism

Objective: To explore the effects of insulin therapy on skeletal muscle wasting (SMW) in severely scalded rats and its related mechanism. Methods: Totally 48 male Wistar rats aged 7-8 weeks were divided into simple scald (SS) group and insulin therapy (IT) group according to the random number table, with 24 rats in each group. After weighing the body mass and measuring the blood glycemic level of the tail end with a glucometer, the rats in the two groups were immersed in hot water at 94 ℃ for 12 seconds to make a full-thickness dorsal scald model involving 30% total body surface area. Rats in group IT were subcutaneously injected with 1 U/kg insulin glargine at 8: 00 a day from post injury day (PID) 1 to 7, whilst rats in group SS were given the same amount of normal saline. Rats in the two groups were given 10 mL/kg enteral nutritional emulsion by intragastric infusion at 8: 00 (after insulin administration), 13: 00, and 18: 00 a day respectively from PID 1 to 7. The blood glycemic levels of tail end of rats in the two groups were measured by glucometer before insulin administration on PID 1-4, 6, and 7 and on every morning of PID 8, 9, 11, 12, and 14. The body mass of rats in the two groups on PID 14 without any treatment was weighed. Eight rats from each group were collected respectively on PID 4, 7, and 14 to harvest tibialis anterior muscle (TAM) samples. The mass of TAM on PID 14 was weighed. The ultrastructural changes of TAM myocytes on PID 7 were observed with transmission electron microscope. The apoptotic rates of TAM myocytes on PID 4, 7, and 14 were assessed by the assay of terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphate-biotin nick end labeling, the expressions of cysteine-aspartic protease-3 (caspase-3) of TAM on PID 4, 7, and 14 were detected with immunohistochemistry, and protein expressions of endoplasmic reticulum (ER) stress (ERS) associated proteins glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein-homologous protein (CHOP), and activated caspase-12 of TAM on PID 4, 7, and 14 were detected with Western blotting. Data were processed with completely random design t test, analysis of variance for repeated measurement, analysis of variance for factorial design, t test, and Bonferroni correction. Results: The blood glycemic level and body mass of rats in the two groups before injury were similar (t=0.204, 0.405, P>0.05). There were no statistically significant differences in blood glycemic levels of rats between the two groups on PID 1, 6, 9, 11, 12, and 14 (t=0.229, 3.339, 1.610, 0.178, 0.181, 0.079, P>0.05). Compared with those of group SS, blood glycemic levels of rats in group IT were significantly lower on PID 2, 3, 4, 7, and 8 (t=7.245, 4.165, 4.609, 4.018, 3.995, P<0.05 or P<0.01). On PID 14, the body mass and TAM mass of rats in group IT were (271±19) g and (0.47±0.05) g respectively, both obviously higher than (254±12) g and (0.43±0.04) g of group SS (t=2.159, 2.375, P<0.05). On PID 7, nuclear pyknosis and deformation, chromosome misdistribution, and ER swelling in TAM myocytes of rats in group SS were observed; the apoptotic alterations and ER swelling of TAM myocytes were alleviated in rats of group IT as compared with those of group SS. The apoptotic rates of TAM myocytes of rats in group IT were obviously lower than those of group SS on PID 4, 7, and 14 (t=4.262, 9.153, 9.799, P<0.01). The expressions of caspase-3 in TAM of rats in group IT were obviously lower than those of group SS on PID 7 and 14 (t=10.429, 7.617, P<0.01). Compared with those of group SS, the protein expressions of GRP78 were obviously increased on PID 4 and 14 (t=4.172, 4.437, P<0.05), the protein expressions of activated caspase-12 were obviously decreased on PID 7 and 14 (t=11.049, 11.181, P<0.01), and the protein expressions of CHOP were obviously decreased on PID 4, 7, and 14 (t=13.837, 9.572, 6.930, P<0.01) in TAM of rats in group IT. Conclusions: Insulin therapy may reduce skeletal muscle myocytes apoptosis and SMW by alleviating ERS in rats with severe scald.

Muramyl Dipeptide Enhances Thermal Injury-Induced Autophagy and Inflammatory Cytokine Response of Lungs via Activation of NOD2/Rick Signaling Pathway in Rats.

Nucleotide-binding oligomerization domain 2 (NOD2) is the innate receptor of muramyl dipeptide (MDP). Our previous study revealed that MDP could enhance thermal injury-induced inflammatory cytokine production and organ function injury in rats. The present study was to determine the effect of MDP on autophagy and NOD2/receptor-interacting serine/threonine protein kinases (RICK) signaling pathway of lung injury after thermal injury. Forty male Sprague-Dawlay rats were randomly divided into four groups: normal control (NC) group, MDP group, Scald group, and MDP + Scald group. Scald group only suffered 20% total body surface area third-degree (TBSA) thermal injury. MDP group was only administered 5.0 mg/kg MDP through the left femoral vein; 5.0 mg/kg MDP was administered through the left femoral vein at 24 h after thermal injury in the MDP + Scald group. TBSA thermal injury (20%) not only significantly increased the plasma inflammatory cytokines production, but also elevated the expression of LC3-I/II, the accumulation of autophagosome in the lung tissue. Compared with the Scald group, MDP + Scald double hit led to more serious inflammatory responses and higher expression of NOD2 mRNA, RICK, NF-κB p65, LC3-I/II, and the accumulation of more autophagosome in the lung tissue. MDP enhances thermal injury-induced autophagy and proinflammatory cytokine response of lung injury, which could be achieved via activating the NOD2/RICK signaling pathway in rats.

Effect of alprostadil on wound healing of scalded rats and the mechanism

Objective: To explore effect of alprostadil on wound healing of scalded rats and the mechanism. Methods: According to random number table method, forty-eight Sprague Dawley rats were divided into sham scald group, simple scald group, lithium chloride group, and alprostadil group, with 12 rats in each group. Rats in sham injury group were sham injured on the back, and rats in the other three groups were inflicted with 30% total body surface area deep partial thickness scald on the back.Immediately after scald, rats in sham scald group and simple scald group were injected with 1 mL saline through caudal vein, and rats in lithium chloride group and alprostadil group were injected respectively with 1 mL lithium chloride and alprostadil through caudal vein. Saline, lithium chloride, and alprostadil were injected once in a day and lasted for 14 days. General wound appearance and wound healing rate on post scald day (PSD) 7, 10, 14 were observed and calculated. Expressions of protein and mRNA of Wnt1 and β-catenin on PSD 14 were detected. Data were processed with analysis of variance of factorial design, one-way analysis of variance, Student Newman Keuls q test, t test, and Bonferroni correction. Results: (1) On PSD 7, wounds of scalded rats in each group formed dry eschar and had little exudation. On PSD 10, wounds of rats in simple scald group were covered with eschar, with little exudation, and wounds of rats in lithium chloride group were covered with eschar, and partial wounds healed under the eschar. On PSD 10, partial eschar of rats in alprostadil group desquamated; partial wounds healed; newly burned skin was ruddy. On PSD 14, partial wounds of rats in simple scald group were healed under eschar with little exudation. On PSD 14, most of the eschar of rats in lithium chloride group were desquamated with patial wounds healed and little exudation. On PSD 14, wounds of rats in alprostadil group were basically healed with vigorously growing hair on the back. (2) On PSD 7, the wound healing rates of rats in simple scald group, lithium chloride group, and alprostadil group were close (F=0.41, P>0.05). On PSD 10 and 14, wound healing rate of rats in lithium chloride group and alprostadil group were significantly higher than that in simple scald group (q=5.73, 17.45, 26.30, 11.28, P<0.05), and wound healing rate of rats in alprostadil group was significantly higher than that in lithium chloride group (q=32.03, 28.73, P<0.05). (3) On PSD 14, the mRNA expressions of Wnt1 and β-catenin of rats in lithium chloride group and alprostadil group were significantly higher than those in simple scald group (q=65.40, 19.16, 66.79, 18.41, P<0.05), and the mRNA expressions of Wnt1 and β-catenin of rats in simple scald group was significantly higher than those in sham scald group (t=14.86, 4.46, P<0.05). (4) On PSD 14, the protein expressions of Wnt1 and β-catenin of rats in lithium chloride group and alprostadil group were 0.98±0.05, 0.98±0.06, 0.97±0.06, and 1.00±0.06, which were significantly higher than 0.49±0.04 and 0.66±0.04 of rats in simple scald group (q=34.62, 22.38, 33.61, 23.47, P<0.05). On PSD 14, the protein expressions of Wnt1 and β-catenin of rats in simple scald group was significantly higher than 0.29±0.03 and 0.31±0.03 of rats in sham scald group (q=14.73, 23.88, P<0.05). Conclusions: Alprostadil can accelerate wound healing through activating Wnt/β-catenin signal pathway and upregulating the expressions of Wnt1 and β-catenin.

Effects of exogenous high mobility group protein box 1 on angiogenesis in ischemic zone of early scald wounds of rats

Objective: To observe effects of exogenous high mobility group protein box 1 (HMGB1) on angiogenesis in ischemic zone of early scald wounds of rats. Methods: Thirty-six Sprague-Dawley rats were divided into HMGB1 group and simple scald (SS) group according to the random number table, with 18 rats in each group. Comb-like copper mould was placed on the back of rats for 20 s after being immersed in 100 ℃ hot water for 3 to 5 min to make three ischemic zones of wound. Immediately after scald, rats in HMGB1 group were subcutaneously injected with 0.4 μg HMGB1 and 0.1 mL phosphate buffer solution (PBS), and rats in SS group were subcutaneously injected with 0.1 mL PBS from boarders of ischemic zone of scald wound. At post scald hour (PSH) 24, 48, and 72, 6 rats in each group were collected. Protein expressions of vascular endothelial growth factor (VEGF) in ischemic zone of wound at PSH 24, 48, and 72 and protein expressions of CD31 in ischemic zone of wound at PSH 48 and 72 were detected by immunohistochemistry. The number of microvessel in CD31 immunohistochemical sections of ischemic zone of wound at PSH 48 and 72 was calculated after observing by the microscope. The mRNA expressions of VEGF and CD31 in ischemic zone of wound were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction at PSH 24, 48, and 72. Data were processed with analysis of variance of factorial design, t test, and Bonferroni correction. Results: (1) At PSH 24, 48, and 72, protein expressions of VEGF in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=7.496, 4.437, 5.402, P<0.05 or P<0.01). At PSH 48 and 72, protein expressions of CD31 in ischemic zone of wound of rats in HMGB1 group were 0.038 8±0.007 9 and 0.057 7±0.001 2 respectively, significantly higher than 0.013 4±0.004 9 and 0.030 3±0.004 0 of rats in SS group (t=10.257, 15.055, P<0.01). (2) At PSH 48 and 72, the number of microvessel in ischemic zone of wound of rats in HMGB1 group was obviously more than that of rats in SS group (t=3.536, 4.000, P<0.05). (3) At PSH 24, 48, and 72, mRNA expressions of VEGF in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=4.406, 3.821, 3.356, P<0.05). At PSH 24 and 48, mRNA expressions of CD31 in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=4.113, 3.466, P<0.05). At PSH 72, mRNA expressions of CD31 in ischemic zone of wound of rats in 2 groups were close (t=0.010, P>0.05). Conclusions: Exogenous HMGB1 can promote angiogenesis in ischemic zone of early scald wounds of rats by increasing expressions of VEGF and CD31.

Relationship between inflammatory responses and autophagy in lung tissues after scald and NOD2 signaling pathway in septic rats

Objective To evaluate the relationship between inflammatory responses and autophagy in lung tissues after scald and nucleotide-binding oligomerization domain-containing protein 2(NOD2)signaling pathway in septic rats. Methods Twenty SPF healthy male Sprague-Dawley rats, weighing 200-250 g, were divided into control group(group C, n=10) and sepsis after scald group(group SS, n=10)using a random number table.The rats were subjected to a third-degree scald burn covering 20% of total body surface area(body surface was shaved and then exposed to 99-100 ℃ water for 12 s), and 24 h later muramyldipeptide 5 mg/kg was intravenously injected to induce sepsis.The rats were only exposed to 20 ℃ water, and 24 h later normal saline 1 ml was given instead in group C. At 6 h after muramyldipeptide injection in group SS and at 6 h after normal saline injection in group C, arterial blood samples were collected for determination of serum tumor necrosis factor-α and interleukin-6 concentrations by enzyme-linked immunosorbent assay.Then rats were sacrificed and lungs were removed for measurement of activity of myeloperoxidase, NOD2 mRNA expression(using real-time polymerase chain reaction)and expression of receptor interacting protein 2, nuclear factor kappa Bp65 and microtubule-associated protein 1 light chain 3Ⅰ(LC3Ⅰ)and LC3Ⅱ in lung tissues(by Western blot). The LC3Ⅱ/Ⅰratio was calculated. Results Compared with group C, the expression of NOD2 mRNA, receptor interacting protein 2 and nuclear factor kappa Bp65 was significantly up-regulated, and the LC3Ⅱ/Ⅰratio and serum tumor necrosis factor-α and interleukin-6 concentrations were increased in group SS(P<0.05). Conclusion The mechanism underlying enhanced inflammatory responses and autophagy in lung tissues during sepsis after scald may be related to activation of NOD2 signaling pathway in rats. Key words: Burns; Sepsis; Nod2 signaling adaptor protein; Autophagy; Inflammation; Lung

Effects of astragalus polysaccharide on cardiac dysfunction in rabbits with severe scald injury

Effects of astragalus polysaccharide on cardiac dysfunction in rabbits with severe scald injury

Is cupping blister harmful?—A proteomical analysis of blister fluid induced by cupping therapy and scald

ObjectiveCupping therapy has a long history in traditional medicine especially in Asian countries. It was controversial whether cupping induced blisters are beneficial to healing effects, and the formation and content in the blisters remain unexplored. We aimed to identify and compare the molecular components of the blister fluid from the cupping therapy and the scalds to explore the necessary of inducing cupping induced blisters. MethodsFluid sample of blisters from fifteen patients receiving cupping therapy (Cupping group) and scald burns (Scald group) were collected in this study. Proteins from the blisters were separated by two-dimensional electrophoresis (2D-gel) and further analyzed by mass spectrometry. In addition, the changes in particular proteins were confirmed by Western blotting. ResultsThe protein components are significantly different between blister from cupping therapy and scalds. The immune responses, oxidative stress and metabolic related proteins (Ig lambda-2 chain C regions, Ig gamma-1 chain C region, hemopexin, prdx2, calmodulin, succinyl-CoA ligase and tetranectin) were increased, whereas the hemoglobin subunit beta was decreased in the Cupping group compared with the Scald group. ConclusionsCupping induced blisters contain several proteins which relate to the activation of certain immune pathways including anti-oxidation, anti-apoptosis, tissue repairing and metabolic regulation. This proteomic analysis may indicate a significant clue to the mechanism study of cupping.

Effects of seawater immersion on the inflammatory response and oxygen free radical injury of rats with superficial partial-thickness scald at early stage

Objective: To study the effects of seawater immersion on the inflammatory response and oxygen free radical injury of rats with superficial-thickness scald at early stage. Methods: Seventy Wistar rats were divided into healthy control group (HC, n=7), pure scald group (PS, n=21), scald+ fresh water immersion group (SF, n=21), and scald+ seawater immersion group (SS, n=21) according to the random number table. Rats in group HC did not receive any treatment, while 5% total body surface area superficial partial-thickness scald was made on the back of rats in the latter three groups. Rats in group PS lived freely immediately post burn, while wounds on the back of rats in groups SF and SS were immersed into fresh water and seawater, respectively. Serum and full-thickness skin tissue in the center of wounds on the back of 7 rats in groups PS, SF, and SS at post immersion (injury) hour (PIH) 2, 4, and 6 were collected, respectively, while serum and full-thickness skin tissue at the same position of the 7 rats in group HC were collected at PIH 6 of rats in other groups. Morphology of skin tissue was observed with HE staining; tumor necrosis factor-alpha (TNF-α) content in serum and skin tissue was determined by enzyme-linked immunosorbent assay; superoxide dismutase (SOD) content in serum and skin tissue was determined by hydroxylamine method; malondialdehyde content in serum and skin tissue was determined by thiobarbituric acid method. Data were processed with analysis of variance of factorial design, one-way analysis of variance, Welch test, LSD test, and Tamhane test. Results: (1) Epidermal cells of skin tissue of rats in group HC arranged in order and continuously, and the dermis tissue and accessory structures were clear and complete. The skin layer and epidermis of wounds of rats in group PS had no significant change, but the edema of epidermis and dermis and infiltration of inflammatory cells enhanced over time at PIH 2, 4, and 6. The horny layer of epidermis of wounds of rats in group SF reduced, and the edema of epidermis and dermis and infiltration of inflammatory cells enhanced over time at PIH 2, 4, and 6; some epidermal cells disintegrated at PIH 6. The horny layer of epidermis of wounds of rats in group SS significantly reduced, along with the increase in disintegration of epidermal cells, the significant enhancement of edema of epidermis and dermis, and infiltration of a large number of inflammatory cells over time at PIH 2, 4, and 6. (2) Compared with (247±27) pg/mL in group HC, the serum content of TNF-α of rats in group PS significantly increased at PIH 2 and 4 [respectively (675±122) and (367±54) pg/mL, P<0.05 or P<0.01] but significantly decreased at PIH 6 [(147±27) pg/mL, P<0.01]; the serum content of TNF-α of rats in group SF significantly decreased at PIH 6 [(90±24) pg/mL, P<0.01]; the serum content of TNF-α of rats in group SS significantly increased at PIH 2, 4, and 6 [respectively (1 646±58), (2 086±114), and (2 951±58) pg/mL, with P values below 0.01]. Compared with (364±123) U/mL in group HC, the serum content of SOD of rats in group PS significantly increased at PIH 2 and 4 [respectively (489±13) and (447±14) U/mL, with P values below 0.05]; the serum content of SOD of rats in group SF significantly decreased at PIH 6 [(282±13) U/mL, P<0.05]; the serum content of SOD of rats in group SS significantly increased at PIH 2 [(461±23) U/mL, P<0.05] but significantly decreased at PIH 4 and 6 [respectively (226±8) and (205±10) U/mL, with P values below 0.01]. Compared with that in group HC, the serum content of malondialdehyde of rats in groups PS, SF, and SS significantly increased at PIH 2, 4, and 6 (with P values below 0.01). (3) Compared with that in group HC, the TNF-α content in wound tissue of rats in groups PS and SS significantly increased at PIH 2, 4, and 6 (P<0.05 or P<0.01), and the TNF-α content in wound tissue of rats in group SF significantly increased at PIH 2 and 4 (with P values below 0.01). Compared with that in group HC, the SOD content in wound tissue of rats in groups PS and SF significantly increased at PIH 2, 4, and 6 (P<0.05 or P<0.01), and the SOD content in wound tissue of rats in group SS significantly increased at PIH 2 and 4 (with P values below 0.01). Compared with that in group HC, the malondialdehyde content in wound tissue of rats in groups PS, SF, and SS significantly increased at PIH 2, 4, and 6 (with P values below 0.01). Conclusions: Seawater immersion can enhance the inflammatory response and oxygen free radical injury of wounds and the whole body of rats with superficial partial-thickness scald at early stage.

Influences of exendin-4 on the secretion function of islet beta cells from rats in the early stage of severe scald

Objective: To observe the secretion function changes of islet beta cells isolated from rats in the early stage of severe scald, and to explore the influence of them. Methods: Thirty-six Wistar rats were divided into sham injury (SI) group, sham injury+ exendin-4 (SIE) group, scald (S) group, and scald+ exendin-4 (SE) group according to the random number table, with 9 rats in each group. Rats in groups S and SE were inflicted with 50% total body surface area full-thickness scald by a 12-s immersion of back and a 6-s immersion of abdomen in 94 ℃ hot water. Rats in groups SI and SIE were sham injured through immersion of back and abdomen in 37 ℃ warm water. Rats in groups S and SE were subcutaneously injected with exendin-4 (4 μg/kg) twice a day post injury, while rats in groups SI and SIE were subcutaneously injected with sterile water in the same volume. At post injury hour (PIH) 72, the following detections were performed. Eight rats of each group were respectively selected to measure level of fasting blood glucose with cutting-tail method, and to detect plasma level of glucagon-like peptide 1 (GLP-1) and serum level of insulin by enzyme-linked immunosorbent assay (ELISA). The insulin resistant index (HOMA-IR) was calculated. Six rats of each group were respectively selected for islet isolation. The isolated rat islets were stimulated with RPMI 1640 medium containing 2.8 or 16.7 mmol/L glucose, respectively. Insulin content in supernatant was detected by ELISA, and insulin secretion index was calculated with 6 samples in each group. The isolated islets from 3 rats of each group were selected for the observation of the super-structure of islet beta cells under transmission electron microscope. The number of docked granules in per 10 μm membrane of islet beta cells and the ratio of insulin vesicles to the total insulin granules were calculated with 3 samples in each group. Data were processed with one-way analysis of variance and LSD test. Results: (1) Compared with that in group S, levels of fasting blood glucose of rats in group SI, SIE, and SE were significantly decreased (P 0.05). Under stimulation of 16.7 mmol/L glucose, compared with that in group SI, the insulin secretion content of rats in groups SIE and SE were significantly increased (P<0.05 or P<0.01), while in group S it was significantly decreased (P<0.05). Compared with that in group SE, the insulin secretion content of rats in group S was significantly decreased (P<0.01) . Compared with that in group S, the insulin secretion content of rats in group SE was significantly increased (P<0.01). Compared with that in group SI (2.25±0.20), the insulin secretion index of rats in group SE (2.68±0.24) was significantly increased (P<0.05). Compared with that in group SIE (2.47±0.18), the insulin secretion index of rats in group S (2.11±0.28) was significantly decreased (P<0.05). Compared with that in group S, the insulin secretion index of rats in group SE was significantly increased (P<0.01). (4) Compared with those in group SI, the number of docked granules per 10 μm membrane of islet beta cells in group SE was significantly increased (P<0.05), while the ratio of insulin vesicles of rat islet beta cells in group S was significantly increased (P<0.01). Compared with those in group SE, the number of docked granules per 10 μm membrane of islet beta cells in group S was significantly decreased (P<0.01), while the ratio of insulin vesicles of rat islet beta cells was significantly increased (P<0.05). Compared with those in group S, the number of docked granules per 10 μm membrane of islet beta cells in group SE was significantly increased (P<0.01), while the ratio of insulin vesicles of rat islet beta cells was significantly decreased (P<0.05). Conclusions: In the early stage of severe scald in rats, level of GLP-1 is decreased and the insulin secretion function of islet beta cells is injured. Long-lasting GLP-1 analogous exendin-4 can improve the secretion function of isolated islet beta cells from severely scalded rats.

Effect of hydrocinnamoyl-L-valyl pyrrolidine on healing quality of deep partial-thickness scald wound in mice

Effect of hydrocinnamoyl-L-valyl pyrrolidine on healing quality of deep partial-thickness scald wound in mice