扶正解毒消积方对二乙基亚硝胺诱导肝癌大鼠核受体共刺激因子5-信号传导与转录激活因子3信号通路的调控机制  

Regulatory effects of Fuzheng Jiedu Xiaoji Formula on the nuclear receptor coactivator 5-signal transducer and activator of transcription 3 signal pathway in rats with hepatocellular carcinoma induced by diethylnitrosamine

作　　者：冯颖 杨雪 孙乐 刘遥 王宪波 FENG Ying;YANG Xue;SUN Le;LIU Yao;WANG Xian-bo(The First Department of Integrative Medicine,Beijing Ditan Hospital,Capital Medical University,Beijing 100015,China)

机构地区：[1]首都医科大学附属北京地坛医院中西医结合一科,北京100015

出　　处：《中华中医药杂志》2020年第7期3711-3714,共4页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：北京市科技计划课题(No.Z191100006619033);首都医学发展基金重点项目(No.2018-1-2172);北京市属医院科研培育计划(No.PZ2016012)。

摘　　要：目的:探讨二乙基亚硝胺(DENA)诱导的肝癌大鼠肝组织中核受体共刺激因子5(NCOA5)的表达改变情况、对信号传导与转录激活因子3(STAT3)磷酸化(p-STAT3)的影响及扶正解毒消积方的干预作用。方法:雄性SD大鼠66只,随机分为正常组、模型组、中药组。模型组及中药组用DENA腹腔注射法诱导肝癌大鼠模型,12周成模后,中药组予扶正解毒消积方灌胃治疗。灌胃3周后处死大鼠,免疫荧光、免疫组化及Western Blot法评估各组大鼠肝组织中NCOA5、STAT3及p-STAT3的表达水平。结果:免疫组化法显示,与正常组比较,模型组大鼠肝脏组织中NCOA5表达降低(P<0.01),STAT3及p-STAT3的表达明显升高(P<0.01);扶正解毒消积方可提高肝癌大鼠肝脏中NCOA5的表达水平(P<0.01),抑制STAT3及p-STAT3的表达(P<0.05),延长大鼠生存时间;Western Blot法结果趋势与其一致。结论:扶正解毒消积方可通过提高NCOA5水平抑制STAT3的磷酸化,从而发挥抗肿瘤的作用。Objective:To investigate the expression of nuclear receptor coactivator 5(NCOA5)in the liver tissue of rats with hepatocellular carcinoma induced by diethylnitrosamine(DENA),and to analyze the effects on signal transducer and activator of transcription 3(STAT3)pathway activation,and evaluate intervention with Fuzheng Jiedu Xiaoji formula(FZJD).Methods:Sixtysix male SD rats were randomly divided into a normal group,a model group,and a FZJD group.Rats in the model and FZJD groups were intraperitoneally injected with DENA for 12 weeks.The rats were killed after three weeks of administration by gavage.The expression levels of NCOA5,STAT3,and p-STAT3 were assessed by immunohistochemistry and Western Blot.Results:Compared to the normal group,the expression of STAT3 and p-STAT3 in the liver tissue of the model group increased(P<0.01)while the expression of NCOA5 decreased(P<0.01).FZJD increased the expression of NCOA5(P<0.01)and decreased the expression of STAT3 and p-STAT3(P<0.05)in hepatocellular carcinoma tissue,thereby prolonging the overall survival time of rats with hepatocellular carcinoma.Conclusion:FZJD may inhibit the activation of STAT3 by regulating NCOA5 in hepatocellular carcinoma.

关 键 词：扶正解毒消积方 二乙基亚硝胺 原发性肝癌 核受体共刺激因子5 信号传导与转录激活因子3 

分 类 号：R285.5[医药卫生—中药学]