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OBJECTIVE:To study the protective effects of Polygonum hydropiper extract on acute gastric mucosal lesion (AGML)in rats. METHODS:48 rats were randomly divided into normal group(normal saline),model group(normal saline), positive group(ranitidine hydrochloride,0.05 g/kg),P. hydropiper extract low-dose,medium-dose and high-dose groups(2.7, 8.1,24.3 g/kg by crude drug),i.g. for consecutive 7 d,once a day. Except for normal group,other groups were given absolute ethyl alcohol to induce AGMI model after 1 h of last administration. 1.5 h after modeling,gastric mucosal lesion index of rats was calculated;the pathological changes of gastric tissue in rats were observed;nuclear factor E2 related factor 2(Nrf2)content and SOD activity in gastric tissue of rats were determined by ELISA. RESULTS:Compared with normal group,the gastric mucosa of model group was damaged obviously,there was blood capillary rupture in submucosa,gastric mucosal lesion index was increased significantly(P<0.01);Nrf2 content and SOD activity were significantly decreased in gastric tissue of rats(P<0.05 or P<0.01). Compared with model group,gastric mucosal lesion of rats was relieved to different extent;in positive group,P. hydropiper extract medium-dose and high-dose groups,gastric mucosal lesion index was decreased significantly(P<0.05),and Nrf2 content and SOD activity were increased significantly(P<0.05 or P<0.01). CONCLUSIONS:P. hydropiper extract has good protective effect on absolute ethyl alcohol-induce AGMI,the mechanism of which may be associated with raising Nrf2 content and enhancing SOD activity in gastric mucosal tissue.
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AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
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AIM:To observe the antiulcer effect of butyric acid and hydrogen , the main metabolites of Clos-tridium butyricum (C.butyricum), and to explore the underlying mechanism .METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol .The mice were randomly divided into 4 groups:normal group , model group , butyric acid group and hydrogen group .The mice in butyric acid group and hydrogen group were given buty-rate and hydrogen prior to model establishment , respectively .Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C.butyricum.Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR.The expression levels of apopto-sis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining .RESULTS:The macroscopic observa-tion found that butyrate , not hydrogen , protected gastric mucosa .HE staining also showed that butyrate significantly attenu-ated the pathological damage of the gastric mucosa induced by ethanol .Compared with model group , the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01).In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased ( P<0.01 ) .CONCLUSION: The gastric mucosa protective metabolite of C.butyricum may be butyric acid , not hydrogen .Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflam- mation and reducing the expression ratio of Bax/Bcl-2.
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Objective To investigate the role of TRPV1 in exacerbation of gastric mucosal injury in a rat water immersion restraint stress (WIRS) model by acute postoperative pain. Methods Thirty Wistar rats were randomly divided into normal controlled group (N group, n=10), WIRS model group (WIRS group, n=10) and surgery after WIRS group (WS group, n = 10). The general extent of gastric mucosal injury was observed and assessed for gastric mucosal ulcer index (UI), intragastric pH and serum SOD/MDA ratio were measured and the expression of TRPV1 mRNA in gastric mocusal was accessed by Real-time Quantitative PCR. Immunohistochemistry was performed to detect the mean density of TRPV1. Results Compared with NC group, WIRS group showed obvious gastric mocusal injure with higher UI , lower values of intragastric pH serum SOD/MDA ratio and TRPV1 (P<0.05). The treatment with surgery after onset of WIRS significantly aggravated the gastric mucusal erosion and hemorrhage, with UI increased (P < 0.05), the value of intragastric pH, serum SOD/MDA ratio and TRPV1 further reduced (P < 0.05). Meanwhile, TRPV1 was inversely correlated with UI, and positively associated with intragastric pH and serum SOD/MDA ratio. Conclusion TRPV1 expression in gastric mocusal of AMGL model is inhibited by acute postoperative pain. TRPV1 may involve in the exacerbation of gastric mucosal injury in WIRS model by acute postoperative pain.
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<p><b>OBJECTIVE</b>To observe the influence of electroacupuncture (EA) at lower-sea points of stomach, large intestine, small intestine and gallbladder on interleukin-1β (IL-1β), high mobility group protein 1 (HMGB 1) and alpha 7 nicotinic acetylcholine receptor (nAchR α7) in rats with acute gastric mucosal lesion (AGML), so as to explore whether there is relative specificity in treating gastric viscera disease by stimulating Zusanli (ST 36).</p><p><b>METHODS</b>Sixty healthy SD rats were randomly assigned into a blank group, a model group, a Zusanli group, a Shangjuxu group, a Xiajuxu group and a Yanglingquan group, ten rats in each one (half male and half female). The WRS method was applied to induce the AGML model except the rats in the blank group. The rats in the blank group were treated with routine diet; the rats in the model group were treated with immobilization at rat platform, 30 min per time; the rats in the Zusanli group, Shangjuxu group, Xiajuxu group and Yanglingquan group were treated with acupuncture and connected with EA device (dilatational wave 10 Hz/50 Hz, positive electrode on the left side and negative electrode on the right side, intensity was appropriate when rat hind leg slightly shook), 30 min per time. The treatment was given once a day. After consecutive 10-day treatment, the gastric tissue was collected and the damage of gastric mucosa was evaluated; ELISA method was applied to measure the content of serum IL-1β and tissue HMGB 1; the Western blot method was applied to measure the expression of nAchR α7 receptor.</p><p><b>RESULTS</b>(1) Compared with the model group, the ulcer index (UI) of gastric mucosa, serum IL-1β and tissue HMGB 1 were lower, and the expression of nAchR α7 was increased in the remaining groups (<0.05,<0.01). (2) Compared with the Zusanli group, the UI of gastric tissue, serum IL-1β and tissue HMGB 1 were higher in the Shangjuxu group, Xiajuxu group and Yanglingquan group (<0.05,<0.01), and the expression of nAchRα7 was reduced in the Yanglingquan group (<0.01).</p><p><b>CONCLUSIONS</b>(1) EA at digestive system-related lower-sea points, through IL-1β, HMGB 1 and nAchR α7, could regulate immune response, lighten inflammatory reaction and reduce mucosal injury, which could realize the intervention effect on AGML rats. (2) From the comparison, it is concluded the intervention effect of Zusanli group is superior to the other groups, partly indicating the relative specificity between Zusanli and stomach.</p>
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Objective To discuss the therapy for acute gastric mucosal lesion(AGML)after pericardial devascularization of advanced schistosomiasis. Methods Fifteen advanced schistosomiasis patients with AGML after pericardial devascularization re-ceived supporting therapy,reducing stomach acid and protecting gastric mucosa therapy,reducing gastric blood flow therapy,en-doscopic spraying topical hemostatic agents or electric coagulation therapy,etc. Results After pericardial devascularization of ad-vanced schistosomiasis,15 patients occurred AGML,and among which,10 cases occurred from 8 to 14 days,and the shortest pe-riod was 5 days and the longest was 23 days. Among the 15 patients,13 patients were cured(86.7%),and 2 died. Conclusion The comprehensive therapy including supporting therapy,reducing gastric acid and protecting gastric mucosa,and endoscopic he-mostasis is effective in the treatment of AGML.
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Objective To discuss the effect of growth hormone(GH) on acute gastric mucosal lesion(AGML) in rats.Methods 120 Wistar rats were divided into four groups randomly: blank control group(n=8),simple model group(n=32),model+rhGH group(n=40) and model+cimetidine group(n=40).Animal models of AGML were set up through soak and tie of rats.GH was injected to the rats in experimental groups,while cimetidine was used in the positive control group.Morphologic changes of rat gastric mucosa in each group were observed and compared on different days(0,4,8,12 d) after stress through gross looking,light microscope,and electron microscope.Ulcer index(UI),secretion amount of gastric acid,pH value and gastric mucosal were compared.Results Compared with blank control and model+cimetidine groups,the histomorphologic changes of gastric mucosa were obviously alleviated in model+rhGH group: only part of epithelial cells swelled,red blood cells were seldom seen,neutrophils infiltration reduced obviously,no remarkable changes were observed in the submucosal tissue.Mucosal cells were in good state and degeneration were seen in only a few cells under the electronic microscope.In addition,UI and the degree of gastric mucosal atrophy in model+rhGH group were lower than that in control group significantly(P
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Objective The aim of this study was to investigate the relationship of gastric mucosal lesions and the parietal oxyntic function in rats under stress as a result of seawater-immersion after open abdominal injury. Methods Thirty-two SD rats were subjected to open abdominal injury followed by seawater immersion. The animals were randomly divided into four groups: control, 1h, 2h, 3h stress for 1h, 2h, and 3h groups. The pH value of gastric juice and gastric mucosal ulcer index (UI) were measured. The gastric mucosal lesions were observed with light microscopy, and the ultrastructural changes in parietal cells were observed by transmission electron microscopy. Results There was a significantly negative relationship between UI and pH value (r=-0.70,P