萎胃康及其拆方治疗慢性萎缩性胃炎的作用机制研究

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目的:研究萎胃康及其拆方对慢性萎缩性胃炎大鼠胃黏膜组织形态学的影响及可能机理。方法:将70只大鼠随机分为正常组和造模组,造模组采用综合造模法,经6周复制病理模型。造模成功的50只大鼠随机分为模型组、全方组、补益组、祛邪组、西药组,分别灌胃生理盐水、萎胃康全方水煎液、拆方I号水煎液、拆方II号水煎液和维霉素混悬液治疗30日,1次/日。H-E染色,光镜下观察用药后各组大鼠胃黏膜组织形态的变化,检测各组大鼠胃黏膜上皮细胞线粒体膜电位、细胞色素C和caspase-9活性的变化。结果:光镜下发现模型组大鼠胃黏膜层不完整、变薄,多数腺体结构紊乱,有不同程度的萎缩或消失,并有淋巴细胞、浆细胞呈灶性或弥漫性浸润。各治疗组大鼠胃黏膜病理明显改善,较模型组有显著性差异,其中以全方组治疗效果最好。模型组大鼠线粒体膜电位表达明显高于正常组(P<0.01),细胞色素C和caspase-9明显低于正常组(P<0.01);各治疗组线粒体膜电位表达明显低于模型组(P<0.01),细胞色素C和caspase-9明显高于正常组(P<0.01),其中以全方组变化最为明显。结论:萎胃康及其拆方能明显修复慢性萎缩性胃炎大鼠胃黏膜,可能与降低细胞线粒体膜电位,从而促进细胞色素C释放和增强caspase-9活性表达,进而促进胃黏膜上皮细胞凋亡有关。 Objective: To investigate the effects of wu wei kang and its decomposed formulas on histomorphology of gastric mucosa in rats with chronic atrophic gastritis and its possible mechanism. Methods: Seventy rats were randomly divided into normal group and model group. The model group was established by synthetic modeling and the pathological model was duplicated for 6 weeks. Fifty rats were randomly divided into model group, Quanfang group, Buyi group, Quxie group and western medicine group. Rats were given normal saline, wuweikang decoction, Decoction I decoction, Side II decoction and doxorubicin suspension for 30 days, 1 time / day. H-E staining. The changes of gastric mucosa morphology were observed under light microscope. The changes of mitochondrial membrane potential, cytochrome C and caspase-9 activity in gastric mucosal epithelial cells in each group were observed. Results: The gastric mucosa of the model group was incomplete and thinned under light microscope. Most of the glandular structures were disorganized with varying degrees of atrophy or disappearance. Lymphocytes and plasma cells were focal or diffuse infiltration. The pathological changes of gastric mucosa of rats in each treatment group were significantly improved, which were significantly different from the model group, of which the treatment effect was the best in the whole prescription group. The expression of mitochondrial membrane potential in model group was significantly higher than that in normal group (P <0.01), while the levels of cytochrome C and caspase-9 in model group were significantly lower than those in normal group (P <0.01) P <0.01), cytochrome C and caspase-9 were significantly higher than the normal group (P <0.01), of which the most obvious changes in all groups. Conclusion: Weweikang and its disassembled prescription can obviously repair gastric mucosa in rats with chronic atrophic gastritis, which may reduce the mitochondrial membrane potential, promote the release of cytochrome C and enhance the expression of caspase-9, and further promote the apoptosis of gastric mucosal epithelial cells Death related.
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