基于PI3K/Akt信号通路探讨抗纤抑癌方干预肝癌前病变的作用机制  

Study on the Mechanism of Kangxianyiai Formula Delay the Occurrence of Hepatic Precancerous Lesions by Regulating the Signal Pathway of PI3K-Akt

作　　者：李莹[1,2] 叶永安[1,2] 李志国[1,2] 张露丹[1,2] 杨先照[2] LJ Ying;YE Yong-an;LI Zhi-guo;YANG Xian-zhao(Dongzhimen Hospital,Beijing University of Chinese Medicine ( Beijing,100700)China)

机构地区：[1]北京中医药大学东直门医院,北京100700 [2]北京中医药大学肝病研究所

出　　处：《中西医结合肝病杂志》2019年第3期240-243,I0004,共5页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases

基　　金：国家自然科学基金青年科学基金项目(No.81603555);北京市自然科学基金青年科学基金项目(No.7174319);北京中医药大学东直门医院第三批“青苗人才”项目(NO.DZMYS-201809)

摘　　要：目的:研究抗纤抑癌方对肝癌前病变大鼠PI3K/Akt信号通路的影响。方法:雄性Wistar大鼠85只,随机分为正常组、模型组、抗纤抑癌低、中、高剂量组及鳖甲软肝组。采用二乙基亚硝胺腹腔注射制备肝癌前病变模型,抗纤抑癌方进行干预,复方鳖甲软肝片作为对照;采用免疫组化法检测GST-Pi的表达,实时荧光定量PCR及Western blot法检测PI3K、Akt mRNA及蛋白的表达。结果:与模型组相比,抗纤抑癌高剂量组GST-Pi阳性表达面积明显减少,染色减轻,MOD值显著降低(P<0.05);与模型组相比,抗纤抑癌低、中、高剂量组及鳖甲软肝组PI3K、Akt mRNA的表达均显著降低(P<0.01),抗纤抑癌低、中、高剂量组PI3K、p-PI3K蛋白表达显著降低(P<0.01或P<0.05),抗纤抑癌中、高剂量组p-Akt蛋白表达显著降低(P<0.01);与鳖甲软肝组相比,抗纤抑癌高剂量组PI3K mRNA及p-PI3K蛋白的表达显著降低(P<0.05)。结论:抗纤抑癌方可通过调控PI3K/Akt信号抑制肝癌前病变。Objective:To discuss the effects of Kangxianyiai Formula on PI3 K-Akt signaling pathway in rats with hepatic precancerous lesions.Methods:Total of 85 male Wistar rats were randomLy divided into normal group, model group, Kangxianyiai Formula low dose, medium dose and high dose group, and Biejiaruangan group. Established the animal models of diethylnitrosamine-induced hepatic precancerous lesions and used Kangxianyiai Formula to treat.Biejiaruangan tablets were taken as control drug.Immunohistochemistry was used to detect the expression of GST-Pi.The expression of PI3 K and Akt mRNA and protein was detected by real-time quantitative PCR and Western blot method. Results:Compared with the model group, the positive expression area of GST-Pi in the high dose group was significantly reduced, the staining was lightened, and the MOD value was significantly decreased(P<0.05).Compared with the model group, the expression of PI3 K and Akt mRNA in the low, middle and high dose group and Biejiaruangan group were significantly decreased(P<0.01).The expression of PI3 K and p-PI3 K protein in the low, middle and high dose groups were significantly decreased(P<0.01 or P<0.05), and the expression of p-Akt protein in the middle and high dose groups were significantly decreased(P<0.01).Compared with Biejiaruangan group, the expression of PI3 K mRNA and p-PI3 K protein decreased in high dose group(P<0.05).Conclusion:Kangxianyiai Formula could delay the occurrence of hepatic precancerous lesions by regulating the PI3 K-Akt signaling pathway.

关 键 词：抗纤抑癌方 肝癌前病变 PI3K AKT GST-PI 

分 类 号：R285.5[医药卫生—中药学]