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目的:观察非酒精性脂肪性肝炎(NASH)大鼠肝组织P65[核因子(NF)-κB亚型]、NF-κB抑制因子(IκB)-α(IκB亚型)蛋白和mRNA情况及杞荷制剂对其影响。方法:采用高脂饮食复制大鼠NASH模型,实验分正常对照组、模型组、杞荷制剂组(大、中、小3个剂量)、复方蛋氨酸胆碱片组。测定各组大鼠肝组织P65、IκB-α蛋白和mRNA的表达。结果:与正常组相比,模型组大鼠肝组织P65、IκB-α蛋白和mRNA明显增强(P<0.01),且P65蛋白主要在胞核分布;与模型组相比,杞荷制剂组大鼠肝组织P65、IκB-α蛋白和mRNA的表达明显降低(P<0.05);复方蛋氨酸胆碱片组大鼠肝组织P65、IκB-α蛋白和mRNA的表达虽有所降低,但与模型组相比差异无统计学意义(P>0.05)。结论:NF-κB蛋白和mRNA表达及NF-κB蛋白活化增强参与NASH的发病;IκB蛋白和mRNA的表达与NF-κB同步增强可能是由共同机制调节的结果;结合NF-κB核移位增强情况,提示NASH状态下IκB氧化磷酸化解离增加,参与了NASH的发病。杞荷制剂能够抑制NF-κB(P65)蛋白和mRNA的表达,同时也可能通过抑制IκB蛋白解离,减少NF-κB的活化及向胞核移位,从而防治NASH。
Objective: To investigate the expression of P65 (NF-κB subtype) and IκB-α (IκB) -type protein and mRNA in non-alcoholic steatohepatitis (NASH) Dutch agents on its impact. Methods: Rat model of NASH was induced by high-fat diet. The rats were divided into normal control group, model group, Qihe preparation group (three doses at large, medium and small doses) and compound methionine choline tablets group. The expression of P65, IκB-α protein and mRNA in the liver of each group were determined. Results: Compared with the normal group, the protein and mRNA of P65, IκB-α in the model group were significantly increased (P <0.01), and the distribution of P65 protein was mainly in the nucleus. Compared with the model group, The protein and mRNA expressions of P65 and IκB-α in rat liver tissue were significantly decreased (P <0.05). The expression of P65 and IκB-α protein and mRNA in the liver tissue of compound methionine choline tablets group was decreased, Compared with no significant difference (P> 0.05). CONCLUSION: NF-κB protein and mRNA expression and activation of NF-κB are involved in the pathogenesis of NASH. Synchronous enhancement of NF-κB and IκB protein and mRNA expression may be mediated by a common mechanism. Situation, suggesting that IκB oxidative phosphorylation dissociation increased in NASH state, involved in the pathogenesis of NASH. Qihao preparations can inhibit the expression of NF-κB (P65) protein and mRNA, and also prevent NASH by inhibiting the dissociation of IκB protein, reducing the activation of NF-κB and translocation to the nucleus.