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Objective:To investigate the effect of Huangqi Jianzhongtang on Janusprotein tyrosine kinase 2/signal transducers and transcriptional activator protein 3 (JAK2/STAT3) signal pathway in rats with spleen-stomach deficiency cold type gastric ulcer (GU). Method:A total of 60 SPF level Wistar rats were randomly divided into two groups: blank group and model group. Model rats were used to reconstruct the spleen-stomach deficiency cold type GU model by comprehensive modeling method. Model rats were divided into model group, Anweiyang group and high, medium and low-dose Huangqi Jianzhongtang groups according to the random number table, with 10 rats in each group. Rats in blank group and model group were given 10 mL·kg-1·d-1 distilled water, and 16, 8, 4 g·kg-1·d-1 Huangqi Jianzhongtang, respectively. Rats in the positive control group were given 0.14 g·kg-1·d-1 Anweiyang for 21 days. The gene expressions of JAK2 and STAT3 in the ulcer tissue were detected by Real-time fluorescent quantitative polymerase chain reaction (Real-time PCR), the protein expressions and phosphorylation levels of JAK2 and STAT3 in the ulcer tissue were detected by Western blot, and the contents of interleukin-10（IL-10）and interleukin-17（IL-17）in the gastric tissue of each group were detected by enzyme-linked immunosorbent assay (ELISA). Result:Compared with the blank group, the general survival condition of the model group was worse, the content of IL-10 in gastric homogenate was significantly reduced, while the content of IL-17 was significantly increased (P<0.05), the protein expressions of JAK2 and STAT3 in gastric tissue was not significantly increased, whereas the gene expressions and phosphorylation levels of JAK2 and STAT3 were significantly increased (P<0.05). Compared with the model group, the content of IL-10 increased, but the content of IL-17 decreased, the gene expressions of JAK2 and STAT3 and the level of protein phosphorylation decreased in the treatment group, especially in the high-dose Huangqi Jianzhongtang group, with statistically significant differences (P<0.05). Conclusion:Huangqi Jianzhongtang can improve the survival condition of rats with spleen stomach deficiency cold type gastric ulcer, and its mechanism may be related to the intervention of gastric mucosal immune barrier dysfunction mediated by JAK2/STAT3 pathway activation.
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OBJECTIVE： To study the repair effect of artificial Isaria cicadae on intestinal mucosal injury induced by 5-fluorouracil （5-FU） in rats. METHODS： Forty SD rats were randomly divided into normal group （normal saline）， model group （normal saline）， artificial I. cicadae high-dose， medium-dose and low-dose groups （3.5， 1.75， 0.875 g/kg）， with 8 rats in each group. Except for normal group， other groups were given intraperitoneal injection of 5-FU （0.25 g/10 mL） 30 mg/kg， once a day， for consecutive 5 days. At the same time， each group was given relevant medicine/normal saline intragastrically， once a day， for consecutive 8 d. After medication， body weight of rat was determined in each group. HE staining was used to observe the pathological change of small intestine. The levels of biobarrier-related factor [endotoxin （ET）， D-lactic acid （D-LA）]， immune barrier related factors （TNF-α， IFN-γ， sIgA， IL-15， G-CSF in serum and MPO， MDA in small intestine） and the levels of mechanical barrier related factors （connexin ZO-1 and Claudin-1） were detected. RESULTS： Compared with normal group， body weight of rats in model group was decreased significantly （P＜0.01）. Intestinal villus exfoliated obviously， the crypt structure was scattered， a large number of inflammatory cells gathered， and intestinal mucosa was seriously damaged. Serum levels of ET and D-LA， the levels of TNF-a， IFN-γ， MPO and G-CSF in serum， MDA level in small intestine were increased significantly （P＜0.01）. Serum levels of sIgA and IL-15 as well as the expressions of ZO-1 and Claudin-1 in small intestine were decreased significantly （P＜0.05 or P＜0.01）. Compared with model group， body weight of rats in artificial I. cicadae high-dose group was increased significantly （P＜0.01）. The pathological changes of the small intestine of rats in each administration group were improved to varying degrees. The intestine morphology of artificial I. cicadae high-dose and medium-dose groups was close to that of the normal group. The levels of and ET， D-LA， TNF-α， IFN-γ， MPO， G-CSF in serum and the level of MDA in intestinal were decreased significantly （P＜0.01）. Serum levels of sIgA and IL-15 in administration groups as well as the expressions of ZO-1 and Claudin-1 in intestinal tissue were increased significantly （P＜0.01）. CONCLUSIONS： Artificial I. cicadae can repair intestinal mucosal damage caused by 5-FU in respects of mechanical barrier， immune barrier， biological barrier.
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Objective: To investigate effect of Shaoyaotang on intestinal mucosal immune barrier induced by 2,4,6-trinitrobenzene sulphonic acid (TNBS) in rats with ulcerative colitis.Method: Sixty SD rats were randomly divided into normal group,model group,mesalazine group (0.067 mg·kg-1),low,medium and high-dose Shaoyaotang groups (1.8,3.6,7.2 g·kg-1).In the TNBS-induced ulcerative colitis model,saline,mesalazine,peony soup were administered by gavage for 7 days.Hematoxylin-eosin (HE) staining was used to detect the histopathological changes of colon tissue.The number of CD4+T lymphocytes and the expression of secretory immunoglobulin A (SIgA) in intestinal mucosa were detected by immunohistochemistry and Western blot.Result: Compared with normal group,the scores of intestinal mucosal injury and the pathological scores in model group increased significantly (P+T lymphocytes and SIgA in the intestinal mucosa of model group decreased significantly (PP+T lymphocytes and SIgA in the intestinal mucosa of rats in each group elevated significantly (PPP+T lymphocytes and SIgA protein in the intestinal mucosa of rats in middle and high doses Shaoyaotang groups increased significantly (PConclusion: Shaoyaotang can reduce the intestinal mucosal damage and protect the intestinal mucosal immune barrier by increasing the number of CD4+T cells and the expression of SIgA secretion in the intestinal mucosa.
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Aim To study the therapeutic effect of Huangqi Jianzhong decoction ( HQJZ) on duodenal ul-cer(DU) in rats and its effect on intestinal mucosal immune barrier function mediated by TLR-2. Methods SD rats were divided into normal group, model group, positive drug group and HQJZ group. DU model was established by methods of multiple factors. The body weight, food intake, and rectal temperature were measured. The ulcer index (UI) was calculated. The pathological changes of duodenal mucosa were observed by HE staining. The contents of cytokines were detec-ted by EL1SA. The expression of mRNx
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Intestinal mucosal barrier can prevent harmful substances in the intestinal cavity, such as pathogenic microorganisms, biological macromolecules, and antigens into the blood circulation to maintain human health. The adhesion, colonization, and reproduction of normal microbiota in a particular part of the human body can form a layer of “membrane barrier” which is an important defense against the colonization of foreign microorganisms and plays an important role in protecting the body tissue from the invasion of foreign pathogens. Under certain circumstances, such as shock, ischemia, and pancreatitis, the increase in the permeability of intestinal mucosa further leads to intestinal bacterial and endotoxin translocation and release of a large number of proinflammatory cytokines. Therefore, aggravating the primary disease can trigger systemic inflammatory response, insulin resistance, central nervous system damage, and even induce multiple organ failure. Chinese materia medica (CMM) has a clear advantage in the treatment of disorders of intestinal mucosal barrier dysfunction, but most of its effective composition have low bioavailability. After oral administration, CMM can contact with intestinal flora and interact with each other to regulate body-related functions. This article summarizes the effect of CMM on intestinal mucosal barrier through regulating intestinal flora from four aspects which are mechanical barrier, immune barrier, microbial barrier, and chemical barrier of intestinal mucosa, in order to provide references for the research on the regulation of gut microbiota by CMM in the treatment of intestinal mucosal barrier dysfunction-related diseases.
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Objective To explore the correlation between intestinal mucosal immune barrier and pathogenesis of pigment gallstone and its possible mechanism.Methods Eighty guinea pigs were randomly divided into control group(group CON),pigment gallstone group(group PS),and intestinal mucosal protection group(group GLN).The guinea pigs were fed with normal diet in group CON,pigment gallstonein during diet in group PS,and glutamine-supplemented diet in group GLN for 8 weeks.The guinea pig model of pigment gallstone was established.The incidence of pigment gallstone was detected.The morphology of intestinal mucosa was observed,and the numbers of CD3~+T cell,CD40~+B cell,and IgA~+ plasma cell were counted.Results The incidence of pigment gallstone was significantly higher in group PS than in groups GLN and CON(P＜0.05).Compared with group CON,the intestinal wall was significant thinner and represented obvious signs of inflammation in group PS,and the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+ plasma cell significantly decreased(CD3~+ T cell,21.8±2.5 vs 11.1±3.4,P＜0.01;CD 40~+B cell,12.9±2.0 vs 10.7±3.6,P＜0.01;IgA~+ plasma cell,12.4±3.4 vs 10.7±3.5,P＜0.01).The signs of inflammation were less severe in group GLN than in group PS.There were significant differences in the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+plasma cell between groups GLN and PS.Conclusion Intestinal barrier dysfunction,including mechanical barrier and immune barrier,is involved in the formation of pigment gallstone.Glutamine has proved to improve the function of intestinal mucosal barrier and decrease the incidence of pigment gallstone.
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The pathogenesis of post- infectious irritable bowel syndrome(PI-IBS)involves abnormal intestinal immune barrier, which possibly includes the pathological aspects: Intestinal and systemic changes in T lymphocyte; the change of inflammatory cytokines; a increase in intestinal mast cells and enterochromaffin cells and so on. Treatment by western medicine based largely on symptomatic treatment. TCM thinks that the fundamental organ of the irritable bowel syndrome is the liver. Emotional factors inducing liver dysfunction lead to the symptoms of irritable bowel syndrome. The pathogenesis of IBS is, the disorder of movement of qi in liver and spleen. Stagnation of liver-QI with deficiency of the spleen or disharmony between liver and spleen is the key pathogenesis of post-infectious irritable bowel syndrome. On this basis, in various stages of the disease, there may be a different pathogenesis. As a special type of IBS, the balance of vital qi and evil factors determine the disease progression of PI-IBS, in the treatment course also should not forget dispelling pathogenic factors while strengthening body resistance, tonifying deficiency and removing dampness。