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,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.
AIM: To study the effect of EGb on the expression of NF-κB and to investigate the main mechanism of Egb in protec-tion of liver fibrosis.METHODS: The rat liver fibrosis model was induced bythe intraperitoneal injection of 400mL/L CCl4 twice a weekfor 8 weeks. All rats were divided into five groups: normalcontrol (10 rats), model group (15 rats), three groups withdifferent dosage of EGb (45 rats). During the course threeEGb groups were given 0.5g/kg, 1.0g/kg, 2.0g/kg EGb bystomach every day, respectively. Expression of NF-κBP65,and α-SMA was detected by immunohistochemistry. SerumHA was detected by radioimmuno-assay. Liver tissue Hyp,MDA, SOD, GSH-Px and serum AST and ALT were alsoexamined.RESULTS: The levels of serum ALT, AST, HA in EGb groupswere obviously lower than these of 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±595.1 vs 3847.4±691.8; HA: 130.9±17.0, 78.2±11.3, 80.3±10.2 vs 160.2±38.7; P <0.05 or P <0.01). SOD and GSH-Px activity ofhepatic tissue in EGb groups were significantly higher thanthose in model group (SOD: 18.5±4.8, 20.9±3.7, 25.3±4.7vs 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). The contents of MDA and Hypwere significantly different in model group from those inEGb groups (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). H-E staining showed that thedegree of liver fibrosis in EGb groups was slighter than thatof model group. Compared with model group, the levels ofNF-κBP65 and α-SMA expression in EGb groups were alldecreased (NF-κBP65: 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 or P <0.01).CONCLUSION: EGb is able to inhibit the induction of NF-κB on HSC activation, which may be related to resistingoxidative stress. This may be one of the main mechanismsof EGb in protection of liver fibrosis in r
出处
《世界华人消化杂志》
CAS
2002年第8期922-926,共5页
World Chinese Journal of Digestology
