全反式维甲酸联合苦参素对大鼠肝癌演进中E-cadherin表达的影响

目的:探讨全反式维甲酸(ATRA)联合苦参素(OMT)干预大鼠肝癌演进中E-cadherin表达的变化.方法:用ATRA和OMT对SD大鼠肝癌变动物模型进行干预,分批处死取材,病理分级后,用免疫组化及Western blot法检测E-cadherin表达的变化.结果:在癌变及药物干预进程中,E-cadherin的表达均逐渐下降,且干预组E-cadherin的表达总是略高于诱癌组,且表达部位从肝细胞膜逐渐转移至细胞浆;尤其是从腺瘤样增生(AH)至胆管细胞癌(CCC)期,诱癌组E-cadherin的表达极显著低于对照组(P<0.05,P<0.01),在AH和CCC期时,干预组E-cadherin的表达极显著高于诱癌组(P<0.01).结论:ATRA和OMT可延缓大鼠肝癌变进程中E-cadherin表达的降低,提示ATRA和OMT可在一定程度上推迟肝癌的发生发展.

Effect of All-trans Retinoic Acid and Oxymatrine on E-cadherin Expressions During the Development of Rat Liver Cancer

Objective:To explore the changes of E-cadherin expressions in the development of rat liver cancer under the intervention of all-trans retinoic acid(ATRA)and oxymatrine(OMT).Methods:On the basis of establishing the animal model of SD rat liver cancerization,ATRA and OMT were given by gavage at the same time.After respectively harvest with batches,pathological grading,immunohistochemistry and Western blot were used to analyze the E-cadherin expressions.Results:In the process of cancerization and ATRA and OMT intervention,E-cadherin expressions were gradually decreased and always higher than the corresponding treatment group.Its distribution changed from hepatocyte membrane to cytoplasm.Moreover,E-cadherin in DENA group was significantly lower than that in the control group(P<0.05,P<0.01)from adenomatous hyperplasia(AH)to cholangiocellular carcinoma(CCC);E-cadherin in treatment group was significantly higher than that in DENA group(P<0.01)from AH to CCC.Conclusion:ATRA and OMT can inhibit the down-regulations of E-cadherin in the process of liver cancerization and could delay the hepatocarcinogenesis and development of liver cancer.