基于蛋白激酶B/雷帕霉素靶蛋白通路观察化浊解毒方对胃癌前病变大鼠肿瘤血管新生机制的影响

摘要

Objective observe the influence of Eliminate turbid fluid and remove toxic formula on tumor neovascularization in precancerous lesions of gastric cancer (PLGC) rats based on AKT /mTOR pathway.Methods 48 male PLGC rats were randomly divided into normal group, model group, retinoic acid remedy group and Eliminate turbid fluid and remove toxic formula group, 12 rats in each group.PLGC model was duplicated by the method of establishment of precancerous lesions of gastric cancer rats.After modeling, the model and normal groups were given 0.9% sodium chloride injection 10 mL/kg, the retinoic acid remedy group received retinoic acid 40 mg/kg, and the Eliminate turbid fluid and remove toxic formula group received Eliminate turbid fluid and remove toxic formula decoction 10 g/kg, successive perfusion 1 time per day for 16 weeks.The protein kinase B (AKT) and mammalian target of rapamycin (mTOR) of PLGC rats' gastric mucosa was observed by immunohistochemical assay.Results After 16 weeks administration, the expressions of AKT and mTOR in model group were higher than those in normal group, with statistical differences (P<0.05).As compared with model group, the expressions of AKT and mTOR in Eliminate turbid fluid and remove toxic group and retinotic acid remedy group were decreased in varying degree,with statistical differences (P<0.05).The expressions of AKT and mTOR in Eliminate turbid fluid and remove toxic formula group were obviously lower than retinoic acid remedy group, with statistical differences (P<0.05).Conclusion Eliminate turbid fluid and remove toxic formula can reverse PLGC through down-regulate expression of AKT and mTOR, regulating the AKT/mTOR pathway and resisting tumor neovascularization.%目的 基于胃黏膜组织蛋白激酶B/雷帕霉素靶蛋白(AKT/mTOR)通路观察化浊解毒方对胃癌前病变(PLGC)大鼠肿瘤血管新生机制的影响.方法 将48只雄性SD大鼠按随机分组法分为正常组、模型组、维甲酸组、化浊解毒组,每组12只.采用胃癌前病变模型的建立法复制PLGC模型成功后,模型组、正常组给予0.9%氯化钠注射液10 mL/kg,维甲酸组予维甲酸药液40 mg/kg、化浊解毒组予化浊解毒方水煎液10 g/kg,均每日1次灌服,连续16周.采用免疫组织化学法,检测化浊解毒方对PLGC大鼠胃黏膜组织AKT、mTOR的影响.结果 给药16周后,模型组AKT、mTOR表达高于正常组,比较差异有统计学意义(P<0.05);与模型组比较,化浊解毒组、维甲酸组AKT、mTOR的表达均有不同程度下降,比较差异有统计学意义(P<0.05);化浊解毒组与维甲酸组比较,AKT、mTOR表达明显降低,比较差异有统计学意义(P<0.05).结论 化浊解毒方可能是通过降低AKT、mTOR的表达,从而调控AKT/mTOR通路,达到抗肿瘤血管新生以逆转PLGC的治疗效果.