解毒化浊和胃方阻断大鼠CAG癌前病变的分子生物学机制

目的探讨解毒化浊和胃方阻断大鼠慢性萎缩性胃炎(CAG)癌前病变(PLGC)发展的分子生物学机制。方法将60只大鼠分为空白对照组15只,模型对照组15只,中药组15只,西药组15只,除空白对照组外,各组以甲基亚硝基胍造模,模型对照组给予双蒸水灌胃,中药组给予解毒化浊和胃方灌胃,西药组给予叶酸灌胃。采用免疫组化及原位分子杂交标记的方法测EGFR蛋白翻译和mRNA转录水平以及病变黏膜组织中增殖细胞核抗原(PCNA)、H-ras癌基因蛋白表达情况。结果模型对照组眦组织EGFR蛋白翻译和mRNA转录均有表达.表达随病变的进展而递增;中药组EGFR蛋白及mR- NA的表达下调,PCNA指数、H-ras癌基因蛋白阳性指数明显低于模型对照组(P<0.05)。结论解毒化浊和胃方对大鼠PLGC细胞的增殖有良好的阻断作用,该作用可能与下调PLGC组织EGFR蛋白及mRNA的表达有关。

The molecular biological action mechanism of Jieduhuazhuohewei decoction in blocking chronic atrophic gastritis and precancerous lesions in rats

Objective To investigate molecular biological action mechanism of Jieduhuazhuohewei decoction in blocking chronic atrophic gastritis(CAG)and precancerous lesions of gastric cancer(PLGC).Methods 60 Wistar rats were divided randomly into 4 groups:blank control group,model control group,TCM group,western drug group,15 rats in each group.Besides blank control group,the rats in other 3 groups were treated with MNNG to estab- lish the models.The rats in model control group were given double distilled water by gavage,the rats in TCM group were given Jieduhuazhuohewei decoction by gavage,while the rats in western drug group were given folacin by garage. The concentrations of EGFR were measured in all the groups.The expressions of EGFR were measured by RT-PCR. Proliferative cell nucleus antigen(PCNA),apoptosis index,change of expression of H-ras in slices of precancerous morbid tissues of gastric mucosa were measured after application of these drugs.Results The concentration of EGFR of TCM group and western drug group were significantly lower than those of model control group(P<0.05),the ex- pression of EGFR in TCM group was obviously lower than that of model control group.The expressions of PCNA and H- ras in TCM group decreased remarkably,which were significantly different from those of other groups(P<0.01 or P<0.05).Conclusion Jieduhuazhuobewei decoction has blocking effect on the proliferation of PLGC cells of rats. which may related with the down-regulation of the expression of EGFR and mRNA of PLGC tissues.