Intestinal Mucosal Barrier In Rats Research Articles

Effects of electroacupuncture with "intestinal disease prescription" on NLRP3 inflammasome and intestinal mucosal barrier in rats with acute ulcerative colitis.

To observe the effects of electroacupuncture (EA) with "intestinal disease prescription" on the intestinal mucosal barrier and NLRP3 inflammasome in rats with dextran sulfate sodium (DSS)-induced acute ulcerative colitis (UC), and explore the underlying mechanism of EA with "intestinal disease prescription" for the treatment of UC. Thirty-two healthy male SPF-grade SD rats were randomly divided into a blank group, a model group, a medication group, and an EA group, with 8 rats in each group. Except for the blank group, the UC model was established by administering 5% DSS solution for 7 days. After modeling, the rats in the medication group were treated with mesalazine suspension (200 mg/kg) by gavage, while the rats in the EA group were treated with acupuncture at bilateral "Tianshu" (ST 25), "Shangjuxu" (ST 37) and "Zhongwan" (CV 12), with the ipsilateral "Tianshu" (ST 25) and "Shangjuxu" (ST 37) connected to the electrodes of the EA instrument, using disperse-dense wave, with a frequency of 10 Hz/50 Hz, and each intervention lasted for 20 minutes. Both interventions were performed once daily for 3 days. The general conditions of rats were observed daily. After intervention, the disease activity index (DAI) score was calculated; colon tissue morphology was observed using HE staining; serum levels of pro-inflammatory cytokines (interleukin [IL]-18, IL-1β) were measured by ELISA; protein expression of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and Caspase-1 in colon tissues was detected by Western blot; positive expression of zonula occludens-1 (ZO-1) and Occludin in colon tissues was examined by immunofluorescence. Compared with the blank group, the rats in the model group exhibited poor general conditions, slow body weight gain, shortened colon length (P<0.01), increased DAI score and spleen index (P<0.01), elevated serum IL-18 and IL-1β levels, and increased protein expression of NLRP3, ASC, and Caspase-1 in colon tissues (P<0.01), along with decreased positive expression of ZO-1 and Occludin in colon tissues (P<0.01). Compared with the model group, the rats in the medication group and the EA group exhibited improved general conditions, accelerated body weight gain, increased colon length (P<0.05), reduced DAI scores and spleen indexes (P<0.05), decreased serum IL-18 and IL-1β levels, and lower protein expression of NLRP3, ASC and Caspase-1 in colon tissues (P<0.05), as well as increased positive expression of ZO-1 and Occludin in colon tissues (P<0.05). There were no significant differences in the above indexes between the medication group and the EA group (P>0.05). Compared with the blank group, the rats in the model group exhibited disrupted colon mucosal morphology, disordered gland arrangement, and atrophy of crypts, along with significant inflammatory cell infiltration. Compared with the model group, the rats in both the medication group and the EA group showed relatively intact colon mucosal morphology, with restored and improved gland and crypt structures, and reduced inflammatory cell infiltration. EA with "intestinal disease prescription" has a significant therapeutic effect on DSS-induced UC, possibly by regulating the expression of NLRP3 inflammasome and proteins related to the intestinal mucosal barrier, thereby alleviating symptoms of ulcerative colitis.

Benefit Effect of Dendrobium officinale Ultrafine Powder on DSS-Induced Ulcerative Colitis Rats by Improving Colon Mucosal Barrier.

Materials and Methods After intragastric administration of DOFP for 3 weeks, the rat UC model was made by the administration of 4% oral DSS solution for one week, and the drug was given at the same time. During the experiment, the disease activity index (DAI) score of the rats was regularly computed. At the end of the experiment, the blood routine indexes of rats were obtained. The histopathological changes in the colon were monitored by hematoxylin-eosin (H&E) and PAS staining and observation of ultrastructural changes in the colon by transmission electron microscope. Occludin expression in the colon was monitored by Western blot, the expression of claudin-1 and ZO-1 in the colon was detected by immunofluorescence, and the expression of TNF-α, IL-6, and IL-1β in the colon was detected by immunohistochemistry. Results The results firstly indicated that DOFP could significantly alleviate the signs and symptoms of the DSS-induced rats UC model, which manifested as improvement of body weight loss, increase of colon length, and improvement of the symptoms of diarrhea and hematochezia. Then, results from histopathology, blood routine examination, and transmission electron microscope analysis further implied that DOFP could dramatically reduce inflammatory cell infiltration and restore intestinal epithelial barrier integrity. In addition, the experiments of Western Blot analysis, immunofluorescence, and PAS staining also further confirmed that DOFP could markedly increase related protein expressions of the intestinal barrier and mucus barrier, as the expression of occludin, claudin-1, and ZO-1 in the colon significantly decreased. The experiments of immunohistochemistry confirmed that DOFP could markedly decrease protein expression levels of inflammatory cytokines TNF-α, IL-6, and IL-1β. Conclusion DOFP notably alleviated inflammatory lesions, repaired the colon mucosa damage by promoting the expression of tight junction proteins occludin, claudin-1, and ZO-1 and inhibiting the release of inflammatory factors TNF-α, IL-6, and IL-1β, and finally achieved the purpose of treating UC.

Toxicokinetics of mono-(2-ethylhexyl) phthalate with low-dose exposure applying fluorescence tracing technique

Di(2-ethylhexyl) phthalate (DEHP) belongs to environmental endocrine disrupting chemicals (EEDCs) and can be rapidly hydrolyzed into the ultimate toxicant mono-2-ethylhexyl phthalate (MEHP). In this study, we used 5-aminofluorescein modified MEHP (MEHP-AF) as a fluorescence tracer to explore the toxicokinetics, including toxicokinetic parameters, absorption and transport across the intestinal mucosal barrier, distribution and pathological changes of organs. While the dose was as lower than 10 mg/kg by intragastric administration, the toxicokinetic parameters obtained by fluorescence microplate method were similar to those with the literatures by chromatography. MEHP-AF can be rapidly absorbed through the intestinal mucosal barrier in rats. In situ organ distribution in mice showed that MEHP-AF was mainly concentrated in the liver, kidney and testis. Our results suggested that the fluorescence tracing technique had the advantages with easy processing, less time-consuming, higher sensitivity for the quantitative determination, In addition, this technology also avoids the interference of exogenous or endogenous DEHP and MEHP in the experimental system. It also can be utilized to the visualization detection of MEHP in situ localization in the absorption organ and the toxic target organ. The results show that this may be a more feasible MEHP toxicological research method.

Protective Role of Somatostatin in Sepsis-Induced Intestinal Barrier Dysfunction through Inhibiting the Activation of NF-κB Pathway.

Somatostatin (SST) has a protective role in intestinal injury, inflammatory response, and intestinal mucosal barrier in rats with acute pancreatitis. However, its function in sepsis-induced intestinal barrier dysfunction remains largely unknown. A mouse sepsis model was constructed, and SST was injected into the tail vein. Then, hematoxylin and eosin staining (HE) was used to detect the intestinal barrier dysfunction. Enzyme-linked immunosorbent assay was used to detect the level of tumor necrosis factor α- (TNF-) α, interleukin- (IL-) 6, and interleukin- (IL-) 10 in the ileum. Expressions of tight junction proteins, zonula occludens- (ZO-) 1 and Claudin-1, and NF-κB p65 in the ileum were detected using western blot and immunohistochemistry as needed. Furthermore, JSH-23 as an inhibitor of the NF-κB pathway was injected into sepsis mice with SST or not. Mice with sepsis showed an obvious intestinal barrier dysfunction with decreasing specific somatostatin receptor subtype (SSTRs), and increasing TNF-α, IL-6, and IL-10 in the ileum. SST could relieve the injury, the decrease of SSTRs, and the increase of TNF-α and IL-6 induced by sepsis and also further enhanced the expression of IL-10. Further analysis showed that ZO-1 and Claudin-1 were reduced in the ileum by sepsis but enhanced by SST. NF-κB p65 was promoted in the ileum by sepsis but inhibited by SST. Further experiments confirmed that NF-κB inhibitor JSH-23 could repair the intestinal barrier dysfunction and enhance the protective effect of SST on the intestinal barrier. SST, with a protective effect on intestinal barrier dysfunction through suppression of NF-κB, could be a potential therapeutic drug for sepsis-induced intestinal barrier dysfunction.

Pingkui Enema Alleviates TNBS-Induced Ulcerative Colitis by Regulation of Inflammatory Factors, Gut Bifidobacterium, and Intestinal Mucosal Barrier in Rats.

Background Ulcerative colitis (UC) is a chronic recurrent inflammation of the colon, and clinical outcome of UC is still unsatisfied. Pingkui enema, a traditional Chinese medicine prescription, has been safely applied for the treatment of diarrhea and dysentery in clinic for many years. However, its mechanism is still elusive. The present study is designed to investigate the effect of Pingkui enema on trinitrobenzene sulfonic acid- (TNBS-) induced ulcerative colitis (UC) and possible mechanism in rats. Methods UC was induced by intracolonic instillation of TNBS in male Sprague-Dawley rats, which were treated with different dosages of Pingkui enema (low, medium, and high) or sulfasalazine for ten days. Survival rate was calculated. A clinical disease activity score was evaluated. Histological colitis severity was analyzed by hematoxylin-eosin (HE) staining. Content of Bifidobacterium in intestinal tissue was analyzed by RT-PCR. Concentration of IL-8, IL-13, TNF-α, D-lactic acid (D-LA), and diamine oxidase (DAO) in serum and contents of adhesin and receptor of Bifidobacterium adhesion in rat intestinal mucus were measured by ELISA. Results The results showed that Pingkui enema treatment with high dosage markedly improved the survival rate compared with untreated and sulfasalazine treated groups. All dosages of Pingkui enema reduced pathological score. High dosage of Pingkui enema and sulfasalazine treatments significantly reduced the serum concentration of IL-8, TNF-α, D-LA, and DAO and markedly increased the serum concentration of IL-13. In addition, high-dose Pingkui enema and sulfasalazine treatments increased gut content of Bifidobacterium, gut mucus expressions of adhesin, and adhesin receptor of Bifidobacterium. Conclusions Pingkui enema has therapeutic effect on TNBS-induced UC, and possible mechanism may be via regulation of gut probiotics (Bifidobacterium) and inflammatory factors and protection of intestinal mucosal barrier.

Protective Effect of Ursolic Acid on the Intestinal Mucosal Barrier in a Rat Model of Liver Fibrosis

Oxidative stress mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) plays an important role in intestinal mucosal barrier damage in various disease states. Recent evidence suggests that intestinal mucosal barrier damage and intestinal dysbiosis occur in mice with hepatic fibrosis induced by CCl4 or bile duct ligation. Another study showed that ursolic acid (UA) attenuates experimental colitis via its anti-inflammatory and antioxidant activities. The goal of this study was to investigate the effects of UA on the intestinal mucosal barrier in CCl4-induced hepatic fibrosis in rats and identify its associated mechanisms. Male Sprague-Dawley rats were randomly divided into the following 3 groups (n = 10/group): the control, CCl4 model and UA treatment groups. Rats were sacrificed at 72 h after the hepatic fibrosis model was established and assessed for liver fibrosis, intestinal injury, enterocyte apoptosis, bacterial translocation, system inflammation, intestinal oxidative stress, and tight junction protein and NOX protein expression. The results demonstrated that UA attenuated the following: (i) liver and intestinal pathological injury; (ii) cleaved caspase-3 expression in the ileal epithelial cells; (iii) serum lipopolysaccharide and procalcitonin levels; (iv) intestinal malondialdehyde levels; and (v) the expression of the NOX protein components NOX2 and P67phox in ileal tissues. Furthermore, our results suggested that UA improved intestinal dysbiosis and the expression of the tight junction proteins Claudin 1 and Occludin in the ileum of rats. These results indicate that UA has protective effects on the intestinal mucosal barrier in rats with CCl4-induced liver fibrosis by inhibiting intestinal NOX-mediated oxidative stress. Our findings may provide a basis for further clinical studies of UA as a novel and adjuvant treatment to cure liver fibrosis.

Enriched environment on the intestinal mucosal barrier and brain–gut axis in rats with colorectal cancer

An enriched environment (EE) is an animal housing technique where animals are given increased amounts of space, physical activity, and social interaction. Presently, researchers studying EEs focus mainly on their effects within the context of neurological diseases. However, little is known about how EEs affect the intestinal mucosal barrier. This study assessed the effects of an EE on the intestinal mucosal barrier in rats with colorectal cancer.

Effects of synbiotics on intestinal mucosal barrier in rat model

Summary Objective To investigate the protective effects of synbiotics on intestinal barrier function, and its priority to probiotics and prebiotics on intestinal barrier function in rat models. Methods We randomly divided 32 rats into four groups: control group (n = 8), probiotics group (n = 8), prebiotics group (n = 8) or synbiotics group (n = 8). All rats received cecectomy and gastrostomy, and tube feeding amoxicillin 50 mg and metronidazole 20 mg on operation day and the first operative day (POD1). After the establishment of impaired intestinal barrier model, rats in the 4 groups received intact protein enteral nutrition, intact protein enteral nutrition+ bifid-triple viable, intact protein enteral nutrition with dietary fiber, intact protein enteral nutrition with dietary fiber+ bifid-triple viable respectively. Samples of blood, urine and tissues of colonic mucose were collected on POD6. Thereafter we measured lactulose/mannitol (L/M) ratio, concentration of certain gut microflora, bacterial translocation rate, endotoxin level of portal vein serum and thickness of colonic mucose. Results Concentration of lactobacilli in probiotics group [(0.828 ± 0.366) × 107 CFU/g] and synbiotics group [(1.424 ± 0.928) × 107 CFU/g] were significantly higher than those in control group [(0.046 ± 0.037) × 107 CFU/g] and prebiotics group [(0.074 ± 0.046) × 107 CFU/g], P L/M ratio in synbiotics group (0.78 ± 0.43) was significantly lower than those in control group (1.45 ± 0.40), probiotics group (1.08 ± 0.22) and prebiotics group (1.35 ± 0.38), P Conclusions Probiotics can improve the concentration of colonic probiotics, while synbiotics can improve probiotics concentration and mucosa thickness in colon, decrease L/M ratio and bacterial translocation. Synbiotics shows more protective effects on intestinal mucosal barrier in rats after cecectomy and gastrostomy and the intervention of specific antibiotics.

Jinhong Tablet Reduces Damage of Intestinal Mucosal Barrier in Rats with Acute Biliary Infection via Bcl-2/Bax mRNA and Protein Regulation.

Objective To explore the effects and mechanism of Jinhong Tablet on intestinal mucosal barrier function and SIRS in rats with acute biliary infection. Methods 36 SD male rats were divided into three groups: sham operation (control), acute biliary infection (ABI) model, and Jinhong Tablet (Jinhong) group. Jinhong group were force-fed with Jinhong Tablet, while the other two groups received oral saline. At days 3 and 5, morphological changes of intestinal mucosa were assessed. Serum diamine oxidase (DAO), D-lactate, and endotoxin levels were measured. And the genes bcl-2 and bax in intestinal tissues were tested by real-time PCR and Western blotting. Results Intestinal damage was significantly less severe in Jinhong group compared with ABI group, as indicated by Chiu's scoring, TUNEL analysis, and serum DAO, D-lactic acid, and endotoxin levels. Additionally, the expression of bax mRNA and protein was decreased and the ratio of bcl-2/bax mRNA and protein was increased compared with ABI group. Conclusion Jinhong Tablet had a positive intervention on acute biliary infection through improving inflammation and intestinal mucosal barrier, inhibiting excessive apoptosis of intestinal epithelial cells via bax and bcl-2 gene, and protein regulation.

Herbal prescription Chang'an II repairs intestinal mucosal barrier in rats with post-inflammation irritable bowel syndrome.

The herbal prescription Chang'an II is derived from a classical TCM formula Tong-Xie-Yao-Fang for the treatment of liver-qi stagnation and spleen deficiency syndrome of irritable bowel syndrome (IBS). In this study we investigated the effects of Chang'an II on the intestinal mucosal immune barrier in a rat post-inflammation IBS (PI-IBS) model. A rat model of PI-IBS was established using a multi-stimulation paradigm including early postnatal sibling deprivation, bondage and intrarectal administration of TNBS. Four weeks after TNBS administration, the rats were treated with Chang'an II (2.85, 5.71 and 11.42 g · kg(-1) · d(-1), ig) for 14 d. Intestinal sensitivity was assessed based on the abdominal withdrawal reflex (AWR) scores and fecal water content. Open field test and two-bottle sucrose intake test were used to evaluate the behavioral changes. CD4(+) and CD8(+) cells were counted and IL-1β and IL-4 levels were measured in intestinal mucosa. Transmission electron microscopy was used to evaluate ultrastructural changes of the intestinal mucosal barrier. PI-IBS model rats showed significantly increased AWR reactivity and fecal water content, and decreased locomotor activity and sucrose intake. Chang'an II treatment not only reduced AWR reactivity and fecal water content, but also suppressed the anxiety and depressive behaviors. Ultrastructural study revealed that the gut mucosal barrier function was severely damaged in PI-IBS model rats, whereas Chang'an II treatment relieved intestinal mucosal inflammation and repaired the gut mucosal barrier. Furthermore, PI-IBS model rats showed a significantly reduced CD4(+)/CD8(+) cell ratio in lamina propria and submucosa, and increased IL-1β and reduced IL-4 expression in intestinal mucosa, whereas Chang'an II treatment reversed PI-IBS-induced changes in CD4(+)/CD8(+) cell ratio and expression of IL-1β and IL-4. Chang'an II treatment protects the intestinal mucosa against PI-IBS through anti-inflammatory, immunomodulatory and anti-anxiety effects.

Effects of simulated microgravity and intravenous moxifloxacin on intestinal mucosal barrier in rats with abdominal infection

Effects of simulated microgravity and intravenous moxifloxacin on intestinal mucosal barrier in rats with abdominal infection

Protective effect of curcumin on intestinal mucosal barrier in rats with obstructive jaundice

Protective effect of curcumin on intestinal mucosal barrier in rats with obstructive jaundice

Influence of dietary fiber complex on intestinal mucosal barrier in rats with portal hypertension

Objective To evaluate the influence of dietary fiber complex (DFC) on intestinal mucosal barrier in rats with portal hypertension.Methods 60 healthy male Wister rat models with portal hypertension established by composite method of CCl4 and olive oil were randomly divided into four groups:group A (simple model group),group B (fed with Nutrison),group C (fed with Nutrison and DFC,SDF∶IDF =1∶2),group D (fed with Nutrison and DFC,SDF∶IDF =2∶1).Then extracted rats' intestinal mucous membrane protein to test the expression of Occludin protein and induced type carbon monoxide synthase (iNOS) on the 7th day.Results The expression of Occludin protein of group C and D increased (P ＜ 0.05),and the expression of iNOS reduced (P ＜ 0.05); the expression of Occludin protein and iNOS had no statistical significant difference between group C and D (P ＞ 0.05).Conclusion DFC has a protective effect on gut barrier in rats with portal hypertension. Key words: Dietary fiber complex; Intestinal mucosal barrier; Portal hypertension; Rat; Occludin protein; Induced type carbon monoxide synthase

Effect of carbachol on intestinal mucosal barrier in rats after diffuse brain injury

Effect of carbachol on intestinal mucosal barrier in rats after diffuse brain injury

Protective effect of exogenous IGF-I on the intestinalmucosal barrier in rats with severe acute pancreatitis.

Severe acute pancreatitis (SAP) can result in intestinal mucosal barrier (IMB) dysfunction. This study was undertaken to demonstrate the effect of IGF-I on the intestinal mucosal barrier in rats with SAP and its possible mechanisms. Seventy-two male Wistar rats were randomly divided into three groups: a sham operation (SO group, n=24), a SAP group not treated with IGF-I (SAP group, n=24), and a SAP group treated with IGF-I (IGF-I group, n=24). SAP was induced in the rats by injecting 5.0% sodium taurocholate into the biliary-pancreatic duct. The SO rats were given an infusion of normal saline instead. The rats in the IGF-I group underwent the SAP procedure and were given a subcutaneous injection of IGF-I at 30 minutes before the operation and at 3 hours after the operation. Eight rats in each group were sacrificed at 6, 12 and 24 hours after operation. Apoptosis of mucosal cells in the small intestine was determined by TUNEL. The levels of endotoxin and DAO and serum amylase were also measured. Pathologic changes in the small intestine were monitored. Changes of bax and bcl-2 mRNA expression in the small intestine were determined by reverse transcription polymerase chain reaction (RT-PCR). The levels of serum amylase were lower in the IGF-I group than in the SAP group at all three time points (P<0.05). The levels of endotoxin in the IGF-I group were higher than those in the SAP group at 6 hours, but lower in the IGF-I group than in the SAP group at 12 and 24 hours (P<0.05). The levels of diamine oxidase were higher in the IGF-I group at 6 hours but lower than those in the SAP group at 12 and 24 hours. The pathological score of the small intestine was lower in the IGF-I group than in the SAP group, and the difference was statistically significant at 12 and 24 hours. The pathologic changes observed under electron microscopy were better in the IGF-I group than those in the SAP group. The apoptosis index of intestinal epithelial cells was significantly decreased in the IGF-I group compared with the SAP group. Compared with the SO group, the mRNA expression levels of bax were increased at each time point in the SAP group, and were significantly decreased in the IGF-I group as compared with the SAP group at each time point (P<0.05). The expression levels of bcl-2 were weak and not different between the SO group and the SAP group (P>0.05). They were significantly increased in the IGF-I group versus the SO and SAP groups (P<0.05). The ratio of bax and bcl-2 mRNA expression levels at each time point in the SAP group were significantly higher than those in the SO group, but they were obviously decreased in the IGF-I group. Exogenous IGF-I seems to protect mucosal cells in the small intestine against SAP-induced apoptosis and could alleviate SAP-induced injury of the intestinal mucosa. The underlying mechanisms include enhanced mRNA expression of bcl-2 and inhibition of bax mRNA expression.

Effects of intestinal mucosal blood flow and motility on intestinal mucosa

To investigate the role of intestinal mucosal blood flow (IMBF) and motility in the damage of intestinal mucosal barrier in rats with traumatic brain injury. Sixty-four healthy male Wistar rats were divided randomly into two groups: traumatic brain injury (TBI) group (n=32), rats with traumatic brain injury; and control group (n=32), rats with sham-operation. Each group was divided into four subgroups (n=8) as 6, 12, 24 and 48 h after operation. Intestinal motility was measured by the propulsion ratio of a semi-solid colored marker (carbon-ink). IMBF was measured with the laser-Doppler technique. Endotoxin and D-xylose levels in plasma were measured to evaluate the change of intestinal mucosal barrier function following TBI. The level of endotoxin was significantly higher in TBI group than in the control group at each time point (0.382±0.014 EU/mL vs 0.102±0.007 EU/mL, 0.466±0.018 EU/mL vs 0.114±0.021 EU/mL, 0.478±0.029 EU/mL vs 0.112±0.018 EU/mL and 0.412±0.036 EU/mL vs 0.108±0.011 EU/mL, P<0.05). D-xylose concentrations in plasma in TBI group were significantly higher than in the control group (6.68±2.37 mmol/L vs 3.66±1.07 mmol/L, 8.51±2.69 mmol /L vs 3.15±0.95 mmol/L, 11.68±3.24 mmol/L vs 3.78±1.12 mmol/L and 10.23±2.83 mmol/L vs 3.34±1.23 mmol/ L, P<0.05). The IMBF in TBI group was significantly lower than that in the control group (38.5±2.8 PU vs 45.6±4.6 PU, 25.2±3.1 PU vs 48.2±5.3 PU, 21.5±2.7 PU vs 44.9±2.8 PU, 29. 4±3.8 PU vs 46.7±3.2 PU) (P<0.05). Significant decelerations of intestinal propulsion ratio in TBI groups were found compared with the control group (0.48%±0.06% vs 0.62%±0.03%, 0.37%±0.05% vs 0.64%±0.01%, 0.39%±0.07% vs 0.63%±0.05% and 0.46%±0.03% vs 0.65%±0.02%) (P<0.05). The intestinal mucosal permeability is increased obviously in TBI rats. Decrease of intestinal motility and IMBF occur early in TBI, both are important pathogenic factors for stress-related damage of the intestinal mucosal barrier in TBI.

Effects of dietary fiber complex on intestinal mucosal barrier in rats with experimental ulcerative colitis

Objective To evaluate the effect of enteral nutrision (EN) containing dietary fiber complex (DFC) on intestinal mucosal barrier in rats with experimental colitis. Methods Ninety six SD rats were induced into ulcerative colitis by acetic acid enema.than were divided into 3 groups. The rats in group C received non-DFC nutrison, while the rats in group Tl or group T2 received soluble dietary fiber (SDF) and insoluble dietary fiber (IDF) of the EN with different proportion (1:2 or 1:3, respectively). At the first-, third-,fifth- and seventh-day after the EN, the concentration of D-lactate and diamine oxidase (DAO) activity in plasma were detected and intestinal samples were obtained to observe the changes of intestinal mucosa. Results At the third-,fifth- and seventh-day,the D-lactate concentration and the DAO activity in plasma significantly reduced in group Tl and T2 when compared with group C (P<0. 05) , but there was no statistical difference between group Tl and group T2. The scores of histological damages of colon in the group Tl and group T2 decreased in comparison with group C at all time points (P < 0. 05). However, the scores of histological damages of colon significantly decreased in group T2 when compared with group Tl at day 5 and day 7 (P <0. 05). Conclusion EN containing DFC may reduce the intestinal permeability of colitis in rats, which has a protective effect on intestinal mucosal barrier. While different proportions of the SDF or IDF ratio result in different effects on the mucosal protection. This protective effect will be enhanced by increasing the ratio of IDF in a certain scale. Key words: Ulcerative colitis; Dietary fiber; Intestinal mucosal barrier) D-lactic acid; Diamine oxidase

Influence of ecoimmunonutrition supplement on intestinal mucosa morphology and gut barrier function in rats after operative stress

To investigate the effects of ecoimmunonutrition supplement on intestinal microecology, epithelial tight junctions, and barrier function in rats with surgical stress. Seventy SD rats after surgical trauma were randomly divided into four groups:(1) placebo group,(2)total parenteral nutrition(TPN) group,(3)enteral nutrition(EN) group and (4)ecoimmunonutrition (EEN)group respectively. Rats received isocaloric and isonitrogenous nutrition. Nutrients were administered via the neck vein and the needle jejunostomy for five days. The homogenated tissues of liver, lung, and mesenteric lymph nodes were cultured to determine the bacterial translocation rate. The transmembrane binding proteins(occludin) was measured by immunohistochemistry. The ultrastructure and morphology of intestinal epithelial tight junctions in the intestine were observed by electron microscope. The feces in cecum was cultured for anaerobic bacterial growth and analysed. The amounts of lactobacteria and bifidobacteria in EEN group were significantly higher than those in TPN group(P<0.05). The expression levels of occludin in the intestine was significantly higher in EEN group than that in TPN and EN group. Furthermore, the intestinal epithelial tight junction and microvilli of EEN group were more intact compared with those of TPN group. The bacterial translocation rates of liver, lung and mesenteric lymph nodes were significantly lower in EEN and EN group than those in TPN group(P<0.05). Application of ecoimmunonutrition can protect intestinal mucosal barrier in rats with operative stress, increase the expression of occludin, maintain the gut epithelial tight junction, and eliminate gut bacterial translocation.

The Protection of Chaishao Chengqi decoction to Intestinal Mucosal Barrier in Rats with severe acute pancreatitis

Objective To observe the protection of Chaishao Chengqi decoction to the intestinal mucosal barrier in rats with severe acute pancreatitis.Methods 72 SD rats were randomly divided into normal control group,SAP group and Chaishao Chengqi decoction therapeutic group.10%L-arginine was injected into the rats abdominal to establish SAP models. Chaishao Chengqi decoction 1ml.kg-1 was injected into the rats' stomach of therapeutic group and repeated injections were given per 6 hours until the rats were executed. Normal control group and SAP group were given isodose stroke-physiological saline solution. Specimens were get at 6,12,24 and 48h for detections:①Pathological change of pancreas and Ileal mucous membrane;②Apoptotic index of Ileal mucous membrane;③TNF-α contents of blood serum. Results Apoptotic index of Ileal mucous membrane in SAP group was significantly higher than Normal control group and therapeutic group(P＜0.05);TNF-α contents of SAP group was significantly higher than normal control group and theraroup(P＜0.05);Pathological lesion of pancreas and Ileal mucous membrane of therapeutic group was slighter than SAP group.Conclusions Our experiment suggested that excessus apoptosis of intestinal mucosa was one of the main mechanisms of mucosal barrier function disorder in SAP. Chaishao Chengqi decoction has a protective effect on the intestinal mucosal barrier function. Key words: Severe acute pancreatitis ; Intestinal mucosal barrier ; Chaishao Chengqi decoction ;