中文摘要：

目的：探讨中药萎胃康对慢性萎缩性胃炎（CAG）大鼠胃黏膜的保护机制。方法：将SD大鼠随机分为正常组、模型组、萎胃康小、中、大剂量组和西药组。造模成功后,正常组和模型组灌胃生理盐水,治疗组灌胃相应药物。30 d后,测各组大鼠体重,TUNEL法测各组大鼠胃黏膜凋亡细胞,免疫组化SP法测胃黏膜NF-κB表达。结果：与正常组比较,模型组大鼠体重明显下降,胃黏膜凋亡细胞数显著增多,NF-κB表达显著升高（P〈0.05）;与模型组比较,各治疗组大鼠体重明显增多,胃黏膜凋亡细胞数和NF-κB表达均显著降低,其中萎胃康大剂量组较小剂量组,体重明显增加,凋亡细胞数和NF-κB表达显著降低（P〈0.05）。结论：萎胃康治疗CAG的机制可能与减少细胞凋亡和炎症反应,促进胃黏膜修复有关。

英文摘要：

Objective ：To discuss the mechanism of Weiweikang protecting gastric mucosal in rats with chronic atrophic. Methods ： Randomly divide SD rats into normal group, model group, Weiweikang small, medium and large dose groups and western medicine group. After the successful modeling, the rats in normal group and model group were treated by normal saline and the rats in the other groups were treated by corresponding medicine. After 30 days,we measured the body weight, detected the apoptosis cells by the TUNEL technology and measured the expression of NF - Kappa B in gastric mucosal by the Technique of immunity group SP in each group. Results ： Compared with the normal group, the body weight of rats in model group was significantly reduced. The number of apoptosis cells and the expression of NF - Kappa B in gastric mucosa in model group were significantly increased（P 〈 0.05 ）. Compared with the model group, the body weights of rats in each treatment group were significantly increased. The number of apoptosis cells and the expression of NF - Kappa B in gastric mucosa in each treatment group were significantly reduced （ P 〈 0. 05 ）. Compared with the Weiweikang small dose group, the body weight of rats in Weiweikang large dose group was significantly in- creased and the number of apoptosis cells and the expression of NF - Kappa B in gastric mucosa in Weiweikang large dose group were significantly reduced（ P 〈 0.05 ）. Conclusion ：The possible mechanism of Weiweikang treating chronic atrophic gastritis is re- ducing the number of apoptosis ceils and the inflammation response to promote repairing the gastric mucosal.