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Objective:To study the role and the mechanism of endotoxin in the pathogenesis of gastric mucosa during portal vein hypertension gastrography(PHG) in the rats with cirrhosis.Methods: Rat model for PHG was established by injection of tetrachloride.The animals were injected with endotoxin i.p.at 3 mg/kg and endotoxin antagonist BPI21 i.v.at 2.0 mg/kg.The plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis factor alpha(TNF-α) was measured with azobenzene and ELISA respectively.Furthermore,the pathological changes of the gastric mucosa were studied with HE stainning.Results:In rats with PHG,increased endotoxin and TNF-αas well as the gastric pathological lesion were observed.Injection of endotoxin remarkably increased plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis TNF-αand induced more serious gastric lesion.Animals injected with endotoxin antagonist BPI21 showed improved gastric mucosal lesion,accompanied by the declining TNF-αlevel.Conclusions:Our results suggestes that endotoxin may play a pathogenetic role in PHG by inducing the expression of TNF-α.
Objective: To study the role and the mechanism of endotoxin in the pathogenesis of gastric mucosa during portal vein hypertension gastrography (PHG) in the rats with cirrhosis. Methods: Rat model for PHG was established by injection of tetrachloride. The animals were injected with endotoxin ipat 3 mg / kg and endotoxin antagonist BPI21 ivat 2.0 mg / kg. plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis factor alpha (TNF-a) was measured with azobenzene and ELISA respectively. Stillrther, the pathological changes of the gastric mucosa were studied with HE stainning. Results: In rats with PHG, increased endotoxin and TNF-α as well as the gastric pathological lesion were observed .jection of endotoxin remarkably increased plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis TNF-α and induced more serious gastric lesion. Animals injected with endotoxin antagonist BPI21 showed improved gastric mucosal lesion, accompanied by the declining T NF-αlevel.Conclusions: Our results suggestes that endotoxin may play a pathogenetic role in PHG by inducing the expression of TNF-α.