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目的:观察维胃方治疗实验性胃溃疡的疗效及其机制。方法:采用冰醋酸制备大鼠胃溃疡模型,各治疗组造模3d后予维胃方高、中、低剂量及雷尼替丁灌胃7d;并设正常组、模型组及对照组。处死大鼠检测胃液pH值、溃疡指数,测定胃黏膜前列腺素E_2(PGE_2)含量,并作组织病理学观察。结果:干预后雷尼替丁组、维胃方高、中、低剂量组溃疡指数明显降低,与模型组、对照组比较,差异有显著性或非常显著性意义(P<0.05,P<0.01);中剂量组降低较雷尼替丁组更明显(P<0.05)。维胃方各剂量组的溃疡抑制率均高于雷尼替丁组。雷尼替丁组、维胃方高、中、低剂量组胃液pH值明显升高,与对照组、模型组比较,差异有显著性或非常显著性意义(P<0.05,P<0.01)。雷尼替丁组、维胃方高、中、低剂量组PGE_2含量升高,与模型组、时照组比较,差异有显著性或非常显著性意义(P<0.05,P<0.01);低剂量组升高较雷尼替丁组更明显(P<0.05)。结论:维胃方对实验性胃溃疡具有明显修复治疗作用。其机制可能通过减少胃酸分泌,增加胃黏膜PGE_2含量,从而在抑制攻击因子和增强防御因子两个环节发挥作用。
Objective: To observe the curative effect and mechanism of weisifang on experimental gastric ulcer. Methods: The rats model of gastric ulcer was prepared with glacial acetic acid. The rats in each treatment group were treated with high, medium and low doses of Weiwei recipe for 7 days and ranitidine for 7 days after modeling. The normal group, model group and control group were also established. Rats were sacrificed to detect gastric juice pH, ulcer index, determination of gastric mucosal prostaglandin E_2 (PGE_2) content, and histopathological observation. Results: After intervention, ulcer index of Ranitidine group and Weitigian high, medium and low dose groups were significantly lower than those of model group and control group (P <0.05, P <0.01) ); The middle dose group decreased more significantly than the ranitidine group (P <0.05). The ulcer inhibitory rate of each dose group of Weidu Fang was higher than that of ranitidine group. The pH value of gastric juice in ranitidine group and Weiwei Fang high, medium and low dose groups was significantly higher than that in control group and model group (P <0.05, P <0.01). The levels of PGE 2 in ranitidine group and Weiwei Fang high, medium and low dose groups were significantly higher than those in model group and shazhao group (P <0.05, P <0.01) The dose group increased more significantly than the ranitidine group (P <0.05). Conclusion: Weisi recipe has obvious healing effect on experimental gastric ulcer. The mechanism may be through the reduction of gastric acid secretion, increased gastric mucosal PGE2 content, thereby inhibiting the attack factor and enhance the defense factor play two roles.