Pathological Changes In Intestinal Mucosa Research Articles

Yinlai Decoction Protects Microstructure of Colon and Regulates Serum Level of D-Lactic Acid in Pneumonia Mice Fed with High-Calorie and High-Protein Diet.

To investigate the effect of Yinlai Decoction (YD) on the microstructure of colon, and activity of D-lactic acid (DLA) and diamine oxidase (DAO) in serum of pneumonia mice model fed with high-calorie and high-protein diet (HCD). Sixty male Kunming mice were randomly divided into 6 groups by the random number table method: normal control, pneumonia, HCD, HCD with pneumonia (HCD-P), YD (229.2 mg/mL), and dexamethasone (15.63 mg/mL) groups, with 10 in each group. HCD mice were fed with 52% milk solution by gavage. Pneumonia mice was modeled with lipopolysaccharide inhalation and was fed by gavage with either the corresponding therapeutic drugs or saline water, twice daily, for 3 days. After hematoxylin-eosin staining, the changes in the colon structure were observed under light microscopy and transmission electron microscope, respectively. Enzyme-linked immunosorbent assay was used to detect the protein levels of DLA and DAO in the serum of mice. The colonic mucosal structure and ultrastructure of mice in the normal control group were clear and intact. The colonic mucosal goblet cells in the pneumonia group tended to increase, and the size of the microvilli varied. In the HCD-P group, the mucosal goblet cells showed a marked increase in size with increased secretory activity. Loose mucosal epithelial connections were also observed, as shown by widened intercellular gaps with short sparse microvilli. These pathological changes of intestinal mucosa were significantly reduced in mouse models with YD treatment, while there was no significant improvement after dexamethasone treatment. The serum DLA level was significantly higher in the pneumonia, HCD, and HCD-P groups as compared with the normal control group (P<0.05). Serum DLA was significantly lower in the YD group than HCD-P group (P<0.05). Moreover, serum DLA level significantly increased in the dexamethasone group as compared with the YD group (P<0.01). There was no statistical significance in the serum level of DAO among groups (P>0.05). YD can protect function of intestinal mucosa by improving the tissue morphology of intestinal mucosa and maintaining integrity of cell connections and microvilli structure, thereby reducing permeability of intestinal mucosa to regulate the serum levels of DLA in mice.

Mechanism of Picrorhizae Rhizoma against functional constipation in mice: an exploration based on 16S rDNA and GC-MS

The study was designed to determine the influences of Picrorhizae Rhizoma on gut microbiota and metabolites in mice with functional constipation(FC). ICR mice were divided into the blank control group, model group, and the low-, middle-, and high-dose Picrorhizae Rhizoma groups. Mice in the model and low-, middle-, and high-dose Picrorhizae Rhizoma groups were modeled with loperamide hydrochloride. After successful modeling, the ones in the low-, middle-, and high-dose Picrorhizae Rhizoma groups were gavaged with Picrorhizae Rhizoma at the corresponding doses for seven days. The first appearance time of tarry stool, the total fecal volume within 3 h, the fecal moisture content, and the intestinal transit rate were observed in each group. The pathological changes in intestinal mucosa were detected by HE staining. The flora dynamics in colon content were measured by 16 S rDNA sequencing, followed by the examination of fecal metabolomic profiles by gas chromatography-mass spectrometry(GC-MS). The results showed that the first appearance time of tarry stool in the model group was prolonged. The total fecal volume within 3 h, the fecal moisture content, and the intestinal transit rate were significantly reduced. The colon tissue showed inflammatory cell infiltration. Gut microflora and fecal metabolites changed dramatically. Picrorhizae Rhizoma alleviated the constipation symptoms, repaired intestinal mucosa, and partially restored the gut microbiota and metabolite compositions in mice with constipation. As demonstrated by intestinal microbiota sequencing, Picrorhizae Rhizoma remarkably reduced the Firmicutes/Bacteroidetes ratio and the relative abundance of Lactobacillus, but increased the relative abundance of Muribaculaceae, Enterorhabdus, and Eggerthellaceae. According to the linear discriminant analysis effect size(LefSe), the dominant bacterial species in the Picrorhizae Rhizoma groups were Muribaculaceae, Dubosiella, and Akkermansia. A total of 43 differential metabolites were detected in the feces of mice, involving the D-glutamine and D-glutamate metabolism, glutathione metabolism, arginine biosynthesis, alanine, aspartate and glutamate metabolism, purine metabolism, and pyrimidine metabolism. All these have demonstrated that Picrorhizae Rhizoma enhanced gastrointestinal motility, protectd gastrointestinal mucosa, and alleviated constipation symptoms possibly by regulating the intestinal microbial communities and metabolites and affecting the related metabolic pathways.

Correlations between inflammatory response, oxidative stress, intestinal pathological damage and intestinal flora variation in rats with type 2 diabetes mellitus.

To explore the correlations between inflammatory response, oxidative stress, intestinal pathological damage, and intestinal flora variation in rats with type 2 diabetes mellitus (T2DM). A total of 80 specific pathogen-free (SPF) male Sprague-Dawley (SD) rats purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijiing, China) were randomly divided into two groups, namely T2DM group (n=40) and normal group (n=40). Then, the contents of inflammatory factors [high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-α (TNF-α)] and oxidative stress indicators [malondialdehyde (MDA) and superoxide dismutase (SOD)] were detected. Meanwhile, the distributions of intestinal florae Bifidobacteria, Escherichia coli, Lactobacilli and Enterococcocci and the variation of endotoxin were compared between the two groups. Besides, colon specimens were pathologically examined to observe the occurrence of chronic inflammation variation, intestinal mucosal erosion, intestinal mucosal wall thickening and intestinal mucosal fibrosis. Next, the influences of the glycosylated hemoglobin on levels of hs-CRP, MDA and endotoxin and colonization ability of intestinal florae were analyzed. Additionally, univariate and multivariate analyses were performed for underlying the relations of the pathogenesis of T2DM in rats with their inflammatory response, antioxidant capacity, endotoxin level and intestinal flora colonization capacity. The levels of hs-CRP and TNF-α were significantly higher in T2DM group than those in normal group (p<0.05). T2DM group exhibited an overtly elevated MDA level (p<0.05), and a clearly lowered SOD level (p<0.05) in comparison with normal group. As to intestinal flora-related indicators, the levels of endotoxin, Escherichia coli and Enterococcocci were evidently higher in T2DM group than those in the normal group (p<0.05), while the levels of Bifidobacteria and Lactobacilli in T2DM group were remarkably lowered (p<0.05). Pathological lesions, including chronic inflammation variation, mucosal erosion, mucosal wall thickening and mucosal fibrosis in intestinal mucosal tissues, were worse in T2DM group than those in the normal group (p<0.05). In T2DM rats, the level of glycosylated hemoglobin was positively correlated with changes in the levels of hs-CRP, MDA and endotoxin (p<0.05), and negatively associated with changes in colonization ability of intestinal florae (p<0.05). Aggravated inflammatory response, decreased antioxidant capacity, increased endotoxin level and weakened colonization ability of intestinal florae were independent risk factors for T2DM in rats. Rats with T2DM have significantly aggravated inflammatory response, weakened antioxidant capacity, imbalanced intestinal florae and markedly pathological changes of intestinal mucosa.

CTGF-mediated ERK signaling pathway influences the inflammatory factors and intestinal flora in ulcerative colitis

ObjectiveTo examine the effect of connective tissue growth factor (CTGF)-mediated ERK signaling pathway on the inflammatory response and intestinal flora in ulcerative colitis (UC). MethodsCTGF expression was determined through immunohistochemistry in UC and colon polyp patients. Dextran sulfate sodium (DSS) was used to construct UC models. Wild-type (WT) and CTGF-deficient (CTGF−/−) mice were randomly divided into WT/CTGF−/− + saline, WT/CTGF−/− + DSS, and WT/CTGF−/− + DSS + U0126 (ERK pathway inhibitor) groups. HE staining was conducted to observe the pathological changes in intestinal mucosa. The quantity of intestinal flora was tested in the feces. ELISA, qRT-PCR, and Western blotting were used to detect related-molecules expressions. ResultsCTGF was up-regulated in the intestinal mucosa of UC patients in relation to the severity and grade. Moreover, UC patients showed enhanced the expressions of p-ERK/ERK and pro-inflammatory factors (IL-1β, IL-6, TNF-α, MPO), increased the quantity of Bacteriodes fragilis (B. fragilis) and Escherichia coli (E. coli), and decreased Bifidobacterium and Lactobacillus. CTGF and pERK/ERK expressions were increased in DSS-induced WT mice, but the pERK expression was lower in CTGF−/− + DSS group than that in the WT + DSS group. U0126 decreased the expressions of pro-inflammatory factors and improved the intestinal flora in WT mice induced with DSS. No significant differences were found in the above indexes between CTGF−/− + DSS group and WT + DSS + U0126 group. ConclusionInhibiting CTGF could improve inflammatory response and intestinal flora to partially reverse DSS-induced UC via blocking ERK signaling pathway.

Evaluation of confocal laser endomicroscopy on pathological changes of intestinal mucosa repairing for patients with ulcerative colitis

Objective To evaluate the advantages of confocal laser endomicroscopy (CLE) for function repairing of ulcerative colitis (UC). Methods Thirty patients with UC who were diagnosed and treated in the First Affiliated Hospital of Zhejiang University Medical College between July 2014 and December 2016 were enrolled in the study group. The control group consisted of 10 patients who were diagnosed as having colonic polyps with colonoscopy and underwent polypectomy in the same period. Both groups were examined with white light endoscopy and CLE, then the fluorescein leakage score was compared. Results There were 10 out of 30 cases in the study group whose whole intestinal mucosa were judged as normal under white light endoscopy. In the other 20 cases, there were parts of intestinal mucosa being judged as abnormal. All of the 10 cases in the control group were with normal colon mucosa. There was a significant difference on fluorescein leakage score by CLE between the study group which showed normal by white light endoscopy and the control group (P 0.05). Conclusion In the process of mucosal healing of UC patients, structural repair can be found firstly through CLE. Mucosal healing under white light endoscopy cannot represent the functional recovery. CLE is more effective than the histopathology in the evaluation of mucosal barrier function. Key words: Colitis, ulcerative; Endoscopy; Fluoresceins; Confocal laser endomicroscopy; Mucosal healing

Intra-abdominal infection combined with intra-abdominal hypertension aggravates the intestinal mucosal barrier dysfunction.

Some patients with intra-abdominal infection (IAI) may develop intra-abdominal hypertension (IAH) during treatment. The present study investigated the impact of IAI combined with IAH on the intestinal mucosal barrier in a rabbit model. Forty-eight New Zealand white rabbits were randomly divided into four groups: (i) IAI and IAH; (ii) IAI alone; (iii) IAH alone; and (iv) Control group. IAI model: cecal ligation and puncture for 48 h; IAH model: raised intra-abdominal pressure (IAP) of 20 mmHg for 4 h. Pathological changes in intestinal mucosa were confirmed by light and scanning electron microscopy. FITC-conjugated dextran (FITC-dextran) by gavage was used to measure intestinal mucosal permeability in plasma. Endotoxin, d-Lactate, and diamine oxidase (DAO) in plasma were measured to determine intestinal mucosal damage. Malonaldehyde (MDA), superoxide dismutase (SOD), and GSH in ileum tissues were measured to evaluate intestinal mucosal oxidation and reducing state. Histopathologic scores were significantly higher in the IAI and IAH group, followed by IAI alone, IAH alone, and the control group. FITC-dextran, d-Lactate, DAO, and endotoxin in plasma and MDA in ileum tissues had similar trends. GSH and SOD were significantly lowest the in IAI and IAH group. Occludin levels were lowest in the ileums of the IAI and IAH group. All differences were statistically significant (P-values <0.001). IAI combined with IAH aggravates damage of the intestinal mucosal barrier in a rabbit model. The combined effects were significantly more severe compared with a single factor. IAI combined with IAH should be prevented and treated effectively.

The effects of lower thoracic epidural blockade on intestinal epithelial barrier and activation of enteric glial cells in rats with hemorrhagic shock and resuscitation

Objective To investigate the effects of lower thoracic epidural blockade on integrity of intestinal epithelial barrier(IEB) and activation of enteric glial cell(EGC) in rats with hemorrhagic shock and resuscitation. Methods Seventy-two SD rats with epidural catheterization according to a modified method described by Bahar et al. were randomly divided into four groups with 18 in each group: sham group(group S), control group(group C), normal saline group(group N) and thoracic epidural blockade group(group T). In group S, rats were just received vascular cannulation, whereas the rats in other groups were subjected to hemorrhagic shock and resuscitation with normal saline according to the modified method described by Wiggers. Thirty minutes before bleeding, either 0.075% ropivacaine(group T) or normal saline(group N) 100 μl/kg was infused through thoracic epidural catheters. The survival rates of rats in 72 h after resuscitation were evaluated. The MAP and HR were monitored after vascular cannulation(T0), 30 min after epidural infusion(T1), 30 min of shock(T2), 60 min of shock(T3), 30 min and 60 min after resuscitation(T4 and T5 respectively). Arterial blood samples were collected for blood gas analysis at T0, T3 and T5. At 3 h following resuscitation, the severity of intestinal edema, the pathological changes of intestinal mucosa, and the function of IEB were evaluated by wet/dry ratio(W/D), Chiu's score, and lipopolysaccharide(LPS) concentrations in the portal vein, respectively. The expression of Occludin and glial fibrillary acidic protein(GFAP), a marker of EGCs, were determined by western blot. Results Compared with group C and group N, the survival rates and median survival time of group T were significantly promoted (P<0.05), While MAP and HR decreased at T4 and T5, the levels of pH and lactic acid at T3 and T5 were alleviated (P<0.05). Besides these, in group T, the levels of W/D, Chiu's score and LPS were decreased while the expression of Occludin and GFAP were increased significantly in comparison with group C and group N(P<0.05). Conclusions Lower thoracic epidural blockade attenuates IEB impairment induced by hemorrhagic shock and resuscitation in rats, alleviating internal environment disturbance and thus promoting survival rates after resuscitation, whose mechanism is related to activation of EGC. Key words: Thoracic epidural blockade; Hemorrhagic shock; Resuscitation; Intestinal epithelial barrier; Enteric glial cell

Experimental study of the influence of Sini decoction on the inflammatory response and the immune function in septic rats

To observe the effect of Sini decoction on inflammatory response and immune function in septic rats and to discuss its possible mechanism. 66 Sprague-Dawley (SD) rats were randomly divided into normal control group (n=6), model group (n=30), and Sini decoction group (n=30). Septic model was reproduced by intraperitoneal injection of lipopolysaccharide (LPS, 5 mg/kg). After the reproduction of sepsis, rats in Sini decoction group received Sini decoction (5 g/kg) by gavage, while those in model group were given equal dose of normal saline in the same way. Rats in normal control group did not receive any treatment. Blood was collected via eye sockets at 2, 12, 24, 48, 72 hours after LPS administration, then the rats were sacrificed. The concentrations of inflammatory mediators, such as interleukin (IL-1, IL-6, IL-10), tumor necrosis factor-α (TNF-α), and the expression level of monocyte human leukocyte antigen-DR (HLA-DR) were determined with enzyme linked immunosorbent assay (ELISA), and the pathological changes in intestinal mucosa were observed under electron microscope. The concentration of IL-1 at 2 hours in model group was gradually increased and peaked at 48 hours (4.07±0.10 ng/L), and then gradually decreased, while the IL-1 level in Sini decoction group peaked at 12 hours (2.98±0.12 ng/L) followed by a gradual decrease. IL-6 in model and Sini decoction groups peaked twice at 12 hours (91.39±1.55 ng/L, 73.00±2.38 ng/L) and 48 hours (82.51±1.49 ng/L, 64.68±1.68 ng/L) respectively. IL-10 in model group gradually decreased after peaking at 2 hours (86.66±6.12 ng/L), and that in Sini decoction decreased at 12 hours (71.61±2.35 ng/L) followed by an increasing tendency, and approached normal level at 48 hours (109.09±4.77 ng/L vs. 124.01±7.89 ng/L, P>0.05). TNF-α in model group was gradually increased and peaked at 48 hours (83.37±3.79 ng/L), and that in Sini decoction peaked at 12 hours (48.52±1.21 ng/L), and decreased to normal level at 72 hours (18.59±1.97 ng/L vs. 15.50±2.68 ng/L, P>0.05). During the course of the experiment, as compared with those of the model group, level of IL-1, IL-6, and TNF-α were significantly lower at all time points in Sini decoction group, and IL-10 was significantly higher. The expression level of HLA-DR in model and Sini decoction groups peaked at 2 hours (4.86±0.15 μg/L, 4.85±0.17 μg/L), and then gradually lowered. HLA-DR expression at 48 hours and 72 hours in Sini decoction group was significantly lower than that in model group (48 hours: 4.21±0.12 μg/L vs. 2.74±0.16 μg/L, 72 hours: 3.80±0.09 μg/L vs. 2.27±0.12 μg/L, both P<0.01). Pathological study of intestinal mucosa showed that the intestinal mucosa were infiltrated significantly by inflammatory cells, and villi were damaged severely in both model group and Sini decoction group at 2 hours after LPS challenge. Infiltration of inflammatory cells in Sini decoction group was less intense after 12 hours, and the intestine villi repair was more obvious compared with model group. Sini decoction could regulate systemic inflammatory response, and promote the repair of intestinal mucosa, the intestinal function and the immune status of septic rats.

Milk Fat Globule-EGF Factor 8 Is a Critical Protein for Healing of Dextran Sodium Sulfate-Induced Acute Colitis in Mice

Milk fat globule-EGF factor 8 (MFG-E8) has been shown to play an important role in maintaining the integrity of the intestinal mucosa and to accelerate healing of the mucosa in septic mice. Herein, we (a) analyzed the expression of MFG-E8 in the gut of wild-type (WT) C57BL/6 (MFG-E8(+/+)) mice with and without dextran sulfate sodium (DSS)-induced colitis, (b) characterized the pathological changes in intestinal mucosa of MFG-E8(+/+) and MFG-E8(-/-) mice with DSS-induced colitis and (c) examined the therapeutic role of MFG-E8 in inflammatory bowel disease by using DSS-induced colitis model. Our data documented that there was an increase in colonic and rectal MFG-E8 expression in MFG-E8(+/+) mice during the development of DSS colitis. MFG-E8 levels in both tissues decreased to below baseline during the recovery phase in mice with colitis. Changes in MFG-E8 gene expression correlated to the levels of inflammatory response and crypt-epithelial injury in both colonic and rectal mucosa in MFG-E8(+/+) mice. MFG-E8(-/-)mice developed more severe crypt-epithelial injury than MFG-E8(+/+) mice during exposure to DSS with delayed healing of intestinal epithelium during the recovery phase of DSS colitis. Administration of MFG-E8 during the recovery phase ameliorated colitis and promoted mucosal repair in both MFG-E8(-/-) and MFG-E8(+/+) mice, indicating that lack of MFG-E8 causes increased susceptibility to colitis and delayed mucosal healing. These data suggest that MGF-E8 is an essential protective factor for gut epithelial homeostasis, and exogenous administration of MFG-E8 may represent a novel therapeutic target in inflammatory bowel disease.

Effect of Tongfu granules and its constituents on barrier function of small intestine in rats with sepsis

To investigate the effects of Tongfu granules and its constituents on barrier function of small intestine in rats with sepsis. The male rats were divided into model group, Tongfu granules group, Rhubarb group and Magnoliae cortex group by random digits table, normal rats as control group. Intraperitoneal injection of lipopolysaccharide (LPS, 6 mg/kg) was used to reproduce sepsis model. After establishment of model, rats in Tongfu granules group were given Tongfu granules 28 g×kg(-1)×d(-1) by gavage, and Rhubarb group and Magnoliae cortex group rats were given Rhubarb or Magnoliae cortex 5 g×kg(-1)×d(-1) by gavage, while the model group was given normal saline in same quantity, once a day. Blood samples of rats were collected at 24, 48, 72 hours for measuring tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) with enzyme linked immunosorbent assay (ELISA). The pathological changes in intestinal mucosa were observed, and the pathological scores was estimated at 72 hours. The levels of TNF-α and IL-8 were significantly higher in model group than those in control group at different time points. The serum levels of TNF-α and IL-8 were significantly lower in treatment groups than those in model group, and the level of TNF-α (ng/L) in Tongfu granules group was significantly lower than that in Rhubarb and Magnoliae cortex groups at different time points (24 hours: 44.64±1.48 vs. 47.18±1.83 and 46.96±2.23, 48 hours: 51.38±1.36 vs. 57.17±2.23 and 59.41±2.01, 72 hours: 55.54±2.58 vs. 64.34±1.02 and 65.96±3.45, all P<0.05), and IL-8 (ng/L) level at 72 hours was significantly lower than that in Magnoliae cortex group (65.53±4.52 vs. 69.14±2.82,P<0.05). The scores of the lesions were significantly higher in model group than that in control group (3.90±0.17 vs. 0). The scores of Rhubarb group, Magnoliae cortex group and Tongfu granules group were 3.15±0.28, 3.18±0.08, and 2.95±0.15, respectively, which were lower than those of the model group (all P<0.01), and the Tongfu granules group descended obviously than other groups. In control group, the intercellular tight junctions were normal, and the morphology of microvilli and mitochondria was also normal. In model group, the microvilli of intestinal mucosa of the small intestine were absent or disintegrated. The intercellular tight junctions were seen to be blurred in Rhubarb and Magnoliae cortex groups, and they were close to normal state in Tongfu granules group. Their integrity was better preserved compared with that of the model group. Injury of barrier function of the small intestine was found in septic rat. It was found that traditional Chinese medicine Tongfu granules, Rhubarb and Magnoliae cortex could protect the barrier function of the small intestine by decreasing the TNF-α and IL-8 levels in septic rats. Above-mentioned effects of Tongfu granules were better than Rhubarb and Magnoliae cortex.

Effects of Dexamethasone and Salvia miltiorrhizae on the Small Intestine and Immune Organs of Rats with Severe Acute Pancreatitis

To observe the protecting effects and mechanisms of Dexamethasone and Salviae miltiorrhizae on intestinal mucosa and immune organs (spleen, thymus and lymph node) in rats with severe acute pancreatitis (SAP). The rats were randomly divided into sham-operated, model control, Dexamethasone treated group and Salviae miltiorrhizae treated group. At 3, 6 and 12 h after operation, the mortality rate, pathological changes of intestinal mucosa and immune organs as well as the contents of serum PAF, IL-1 beta and sIL-2R were observed, respectively. The mortality rate and the contents of PAF (at 3 and 6 h), IL-1 beta (at all time points) and sIL-2R (at 3 and 6 h) as well as the pathological scores of thymus (at all time points) and spleen (at 3 h) in Dexamethasone treated group were significantly lower than those in model control groups (P < 0.05). The contents of PAF (at 3 and 12 h), IL-1 beta (at 6 and 12 h) and sIL-2R (at 3 and 6 h) as well as the pathological scores of thymus (at all time points) and spleen (at 3 and 12 h) in Salviae miltiorrhizae treated group were markedly lower than those in model control groups (P < 0.05). Since both Dexamethasone and Salvia miltiorrhizae can reduce the contents of serum PAF, sIL-2R and IL-1 beta, mitigate the pathological changes in the small intestine, spleen and thymus and reduce the mortality rate of SAP rats, they show good therapeutic effects on SAP rats.

Curative effect of octreotide in the treatment of the intestine harm induced by pancreatitis associated ascetic fluid

Objective To investigate the curative effect of octyeotide in the treatment of the intes tine harm induced by pancreatitis associated ascetic fluid (PAAF) in rats. Methods Forty-eight healthy Sprague-Dawwley (SD) rats were randomly divided into three groups:blank group (A) ,model group (B) and octreotide treatment group (C). PAAF was intraperitoneally injected in groups B and C,and octreotide was given in group C. The levels of serum lipopolysaccharides (LPS) and tumor necrosis factor a (TNF-α) were determined, and those of ATP enzyme and TNF-α were measured in intestinal tissues. The pathological changes of intestinal mucosa were observed. Results Except that the activity of ATP was decreased (P < 0.05) ,the indexes above were all increased (P<0.05) in group A as compared with group B (P<0.05). Except that the activity of ATP enzyme was greatly increased (P <0.05) ,all the other indexes were obviously de creased in group C as compared with group B (P <0.05). Conclusion Octreotide can alleviate the the intes tine harm induced by PAAF. Key words: Pancreatitis; Ascetic fluid; Iintestines; Endotoxin; Octreotide

Protective Effect and Mechanisms of Radix Astragali Injection on the Intestinal Mucosa of Rats with Obstructive Jaundice

Objective. To research the protective effects and mechanisms of Radix Astragali injection on the intestinal mucosa of rats with obstructive jaundice (OJ). Methods. The rats were randomly divided into sham-operated, model control and Radix Astragali treated group. We observed the pathological changes of intestinal mucosa, expression levels of Bax and NF-κB proteins, and apoptosis indexes in intestinal mucosa as well as serum NO, MDA and SOD contents, respectively, on 7d, 14d, 21d and 28d after operation. Results. The pathological severity score (on 7d and 14d), apoptotic indexes (on 14d) of the intestinal mucosa and serum MDA content (on 14d) of treated group were significantly lower than those in the model control group (P < .05). The serum SOD contents (on all time points) of treated group were significantly higher than those in the model control group (P < .05). The sham-operated group (on 21d) of the product of staining intensity and positive rate of Bax protein was significantly lower than model control group (P < .05). Conclusion. Radix Astragali injection could protect the intestinal mucosa of OJ rats by increasing the content of SOD, reducing the content of MDA, inhibiting the apoptosis and relieving the pathological changes of intestinal mucosa.

Effects of Ganoderan on the dysbacteria in intestinal tract of mice

The probiotics and prebiotis as microecological modulator have dramatic effects on the microdysbiosis. We found the effects of Ganoderan (GD) in normal flora in intestinal tract of mice. The mice were divided into normal group, decontaminated (DC) group, GD treated group and Bacillus bifidus praeparatum (LZCL) treated group, in which the three groups were treated per os with Lincomycin to be the DC model. After six‐day treatment, the intestinal flora were detected. Lincomycin decreased the number of Bifidobacterium, Bacteroid and Lactobacillus in intestinal tract of mice. The voltatile fatty acid, acetic acid, propionic acid and butanoic acid in blindgut of mice were decreased, suggesting that the dysbacteria were induced in DC mice. After six‐day treatment, the enteric bacilli and enterococcus of GD treatment group and LZCL group were lower than that of DC group, the Bifidobacterium and Bacteroid of GD treatment Group, while LZCL group were higher than that of DC group. The acetic acid, propionic acid and butanoic acid in blindgut of GD treated group and LZCL group were increased. But the level of acetic acid, propionic acid and butanoic acid in blindgut of DC group were lower than that of normal group. The morphologic data showed that the pathological changes of intestinal mucosa restored to normal state after treatment. These results suggest that the GD is an important microecological modulator.