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目的探讨健脾化瘀解毒复方胃炎I号对胃癌前病变(GPL)的疗效及其分子学机制。方法将SD大鼠随机分为空白对照组,模型组,维酶素组(0.2 g·kg-1),胃炎I号组(7.5 g·kg-1)。采用N-甲基-N’-硝基-N-亚硝基胍(MNNG)水溶液自由饮用、饥饱失常、耗气泻下法复制GPL大鼠模型。观察胃炎I号连续治疗10周后对GPL大鼠Wnt信号通路Wnt1、Wnt3a、细胞周期蛋白D1(Cyclin-D1)表达的影响。结果模型组大鼠胃黏膜上皮的Wnt1、Wnt3a、Cyclin D1表达评分均较空白对照组显著增加(P<0.05,P<0.01);胃炎I号能显著拮抗模型组出现的上述变化(P<0.01)。结论胃炎I号能下调Wnt信号通路Wnt1,Wnt3a,Cyclin D1的表达,抑制Wnt/茁-catenin信号通路的异常激活,能在一定程度上阻断和逆转胃黏膜恶性转变。
Objective To investigate the curative effect and molecular mechanism of Jianpi Huayu Jiedu compound gastritis I on gastric precancerous lesions (GPL). Methods SD rats were randomly divided into blank control group, model group, verapamil group (0.2 g · kg -1) and gastritis I group (7.5 g · kg -1). The GPL rat model was reproduced by drinking freely with N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) aqueous solution. To observe the effect of continuous treatment of gastritis I for 10 weeks on Wnt signaling pathway Wnt1, Wnt3a and Cyclin-D1 expression in GPL rats. Results The expressions of Wnt1, Wnt3a and Cyclin D1 in gastric mucosal epithelium in model group were significantly higher than those in blank control group (P <0.05, P <0.01). Gastritis I significantly inhibited the above changes in model group (P <0.01) ). Conclusion Gastritis I can down-regulate the expression of Wnt1, Wnt3a and Cyclin D1, and inhibit the abnormal activation of Wnt / Zhuo-catenin signaling pathway, which can block and reverse the malignant transformation of gastric mucosa to a certain extent.