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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,1g/kg,2g/kg灌胃,每天1次.8wk末处死大鼠,检测NF-κBP65,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±5.4vs42.1±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-κBP65和α-SMA的表达显著弱于模型组(NF-κBP65:0.173±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.
OBJECTIVE: To study the effect of EGb on NF-κB in rat fibrotic liver and to explore the main mechanism of EGb on hepatic fibrosis. Methods: Rat hepatic fibrosis model induced by CCl4. 70 rats were randomly divided into 5 groups, normal group. 10 animals; 15 model groups; EGb fractions into three groups, 15 in each group; CCl4 treatment in the same model group; EGb solution 0.5 g/kg, 1 g/kg, 2 g/kg gavage once daily for 8 times. At the end of the experiment, rats were sacrificed, and NF-κB P65, α-SMA, SOD, MDA, GSH-Px, HA, Hyp were detected and histopathologically examined. Results: The activity of SOD and GSH-Px in the EGb group was significantly higher than that in the model group. SOD: 18.5±4.8, 20.9±3.7, 25.3±4.7 vs 14.3±3.2; GSH-Px: 48.2±8.1, 50.1±6.8, 51.3±5.4 vs. 42.1±3.9; P<0.05 or P<0.01), while The content of MDA and Hyp was significantly lower than that of the model group (MDA: 2.34±0.29, 2.19±0.45, 2.01±0.17 vs 2.96±0.21; Hyp: 397.2±28.6, 370.2±25.6, 358.4±17.4 vs 499.8±23.5; P< 0.05 or P<0.01), serum ALT, AST, HA were significantly lower than model group (ALT: 2877.2±408.4, 1391.9±655.1, 1527.0±263.4 vs. 4419.2±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 or P<0.01), expression of NF-κB P65 and α-SMA It was weaker than the model group (NF-κB P65: 0.173±0.045, 0.139±0.034, 0.126±0.028 vs 0.212±0.037; α-SMA: 0.183±0.040, 0.174±0.036, 0.141±0.031 vs 0.227±0.045; P<0.05; (P<0.01) HE staining showed that the liver fibrosis in the EGb group was significantly less than that in the model group. Conclusion: EGb attenuates the induction of NF-κB by inhibiting oxidative stress and prevents HSC activation. This may be EGb anti-liver fiber One of the most important mechanisms.