摘要目的:研究Egb对大鼠纤维化肝脏NF-κB的影响,探讨Egb抗肝纤维化作用的主要机制.方法:以CCl4诱导大鼠肝纤维化模型.70只大鼠随机分成5组,正常组10只;模型组15只;Egb组分成三小组,每组15只,CCl4处理同模型组,另分别给予Egb溶液0.5g/kg,lg/kg,2g/kg灌胃,每天1次.8wk末处死大鼠,检测NF-KBP65.α-SMA,SOD,MDA,GSH-Px,HA,Hyp并作病理组织学检测.结果:Egb组肝组织SOD,GSH-Px活性明显高于模型组(SOD:18.5±4.8,20.9±3.7,25.3±4.7vs14.3±3.2;GSH-Px:48.2±8.1,50.1±6.8,51.3±5.4 vs42.1±3.9;P＜0.05或P＜0.01),而MDA,Hyp含量显著低于模型组(MDA:2.34±0.29,2.19±0.45,2.01±0.17vs2.96±0.21;Hyp:397.2±28.6,370.2±25.6,358.4±17.4vs499.8±23.5;P＜0.05或P＜0.01),血清ALT,AST,HA显著低于模型组(ALT:2877.2±408.4,1391.9±655.1,1527.0±263.4vs4419.2±720.1;AST:3257.3±260.1,2358.8±643.5,2065.4±595.1vs3847.4±691.8;HA:130.9±17.0,78.2±11.3,80.3±10.2vs160.2±38.7;P＜0.05或P＜0.01),NF-KBP65和α-SMA的表达显著弱于模型组(NF-KBP65:0.173±0.045,0.139±0.034,0.126±0.028vs0.212±0.037;α-SMA:0.183±0.040,0.174±0.036,0.141±0.031vs0.227±0.045;P＜0.05或P＜0.01).HE染色显示Egb组肝纤维化程度较模型组明显减轻.结论:Egb通过抑制氧化应激而减弱对NF-κB的诱导从而阻止HSC的活化.这可能是Egb抗肝纤维化的重要机制之一.