摘要
目的探索17β-雌二醇(E2)抑制NF-kappa Bp65的表达在四氧化碳(CCl4)诱导Wistar大鼠肝纤维化中肝细胞损伤的意义。方法采用实时荧光定量PCR(SYBR GREEN)技术测量雌二醇治疗的肝纤维化模型大鼠肝脏组织中雌激素受体α(ERα)mRNA和NF-kappa Bp65mRNA的表达;采用免疫组化S-P方法检测肝细胞NF-kappa Bp65和ICAM-1表达并分析与肝细胞损害的关系。结果雌二醇治疗组的肝细胞纤维化模型大鼠ERαmRNA表达高于对照组和他莫昔芬组(P<0.05),而NF-kappa Bp65和ICAM-1表达以及ICAM-1免疫组化表达则低于对照组和他莫昔芬组(P<0.05);雌二醇治疗组的肝细胞损伤的程度也低于对照组和他莫昔芬组。结论E2通过ERα途径抑制NF-kappa Bp65在大鼠肝细胞中的表达,从而减轻了肝细胞的损伤。
Objective To explore the role of 17β-estradiol(E2) in inhibiting expression of NF-kappa Bp65 of rat hepatocyte which had been liver fibrosis induced by carbon tetrachloride(CCl4). Methods The mRNA of both estradiol receptor αand NF-kappa Bp65 were measured using real-time PCR (SYBR GREEN 1) while the expression of NF-kappa Bp65 and ICAM-1 in rat livers were detected by immunohistochemistry. The injury of hepatocytes were evaluated by HE stain. Results The mRNA of estradiol receptor α in liver fibrosis treated by E2 were higher than both control group and group treated by tamoxifen while the mRNA of both NF-kappa Bp65 and ICAM-1 or the protein expression of NF-kappa Bp65 and ICAM-1 were lower than both control group and group treated by tamoxifen. When compared the intensity on injury of hepatocytes between the rat treated by E2 and the rat of control group,it was shown that the intensity on injury of hepatocytes in rat treated by E2 were lower than that of control group or group treated by tamoxifen. Conclusion E2 may inhibit the expression of NF-kappa B P65 to reduce the injury of rat liver fibrosis in way of E2-ERα interaction.
出处
《分子诊断与治疗杂志》
2010年第2期105-111,共7页
Journal of Molecular Diagnostics and Therapy