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目的研究乐胃煎对胃粘膜上皮异型增生大鼠胃粘膜上皮细胞调亡及调控基因（Bcl－2、Fas、ICE）蛋白表达的影响，探讨乐胃煎治疗胃粘膜癌前病变的机制。方法用N-甲基-N-硝基-N-亚硝基肌（MNNG）建立大鼠胃粘膜上皮异型增生模型，设立空白组、造模组、乐胃煎治疗组和维甲酸对照组，对大鼠胃粘膜用TUNEL法检测细胞凋亡，用免疫组织化学法检测Bcl-2、Fas、ICE蛋白表达水平。结果空白组、对照组、治疗组和造模组癌前病变发生率分别为0、26.67％、6．7％和73．33％，治疗组与造模组和对照组比较，差异均有显著性意义（P＜0．05），与正常组对比，差异无显著性意义（P＜0.05）。细胞凋亡指数分别为8．3±3．1、7．8±2．6、7．6±1．9和2．2±0．4，Bcl－2蛋白表达率分别为13．3％、33．3％、20％和66．7％、过量表达率分别为6．7％、6.7％、6．7％和33．3％，治疗组与造模组比较，差异有显著性意义（P＜0．05、P＜0．05），与空白组和对照组比较，差异无显著性意义（P＞0．05、P＞0．05）；Fas蛋白表达率分别为46．7％、40％、46．7％和13．3％、过量表达率分别为13．3％、26．7％、20％和13．3％，治疗组与造模组比较，表达率差异有显著性意义（P＜0．05），过表达率无显著性意义（P＞0．05），与空白组和对照
Objective To study the effect of Lewei decoction on gastric mucosal epithelial apoptosis and the expression of its regulatory genes (Bcl-2, Fas and ICE) in gastric epithelial dysplasia rats, and to explore the mechanism of Lewei decoction in treating gastric precancerous lesions. Methods Rat gastric epithelial dysplasia was established with N-methyl-N-nitro-N-nitrosonitrosin (MNNG). The blank group, model group, Lewei decoction group and retinoic acid control group were established. The apoptosis of rat gastric mucosa was detected by TUNEL method. The expression of Bcl-2, Fas and ICE protein was detected by immunohistochemistry. Results The incidences of precancerous lesions in the blank group, control group, treatment group, and modeling group were 0, 26.67%, 6.7%, and 73.33%, respectively. There was significant difference between the treatment group and the model group and the control group. Sexual significance (P < 0.05), compared with the normal group, the difference was not significant (P <0.05). The apoptotic index was 8.3±3.1, 7.8±2.6, 7.6±1.9, and 2.2±0.4, and the Bcl-2 protein expression rate was 13.3%. , 33.3%, 20%, and 66.7%, overexpression rates were 6.7%, 6.7%, 6.7%, and 33.3%, respectively, and there was a significant difference between the treatment group and the model group. (P<0.05, P<0.05), compared with blank group and control group, there was no significant difference (P>0.05, P>0.05); Fas protein expression rate was 46.7 The percentages of overexpression of %, 40%, 46.7%, and 13.3% were 13.3%, 26.7%, 20%, and 13.3%, respectively. There was a difference in the expression rate between the treatment group and the model group. Significant (P<0.05), over-expression rate was not significant (P>0.05), compared with blank group and control group.