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目的建立大鼠非酒精性脂肪性肝炎(NASH)动物模型,探讨脂质过氧化、一氧化氮(NO)和一氧化氮合酶(NOS)以及肿瘤坏死因子-α(YNF-α)、转化生长因子-β(TGF-β)等细胞因子在 NASH 致病中的作用。方法通过持续16周的高脂肪、高胆固醇饮食,建立大鼠 NASH 模型,造模结束吋检测模型组和正常组血清转氨酶,血清及肝组织丙二醛(MDA)、超氧化物歧化酶(SOD)、NO、NOS、谷胱甘肽(GSH)含量。免疫组化标记α平滑肌肌动蛋白(α-SMA)、KP-1、TNF-α、TGF-β。结果实验结束吋,模型组动物体重、肝脏指数比正常组显著增高(P 值分别<0.05和0.01)。血清转氨酶较正常组显著升高(P<0.01)。除血清 NO 显著升高外(P<0.05),MDA、SOD、NOS、GSH 均与正常组差异无统计学意义(P>0.05);而肝匀浆中,MDA、NO 较正常组显著升高(P 值分别<0.05和<0.01),SOD、NOS、GSH 则较正常组显著下降(P 值分别<0.05和0.01)。模型组α-SMA、KP-1、TNF-α、TGF-β免疫组化显示阳性细胞较正常组显著增加(P 值均<0.01)。结论脂质过氧化损伤增强,抗氧化能力降低,以及 TNF-α、TGF-β、NO 等炎性介质活化,共同参与了 NASH 的发病,并预示 NASH 可发展为肝纤维化、肝硬化。
Objective To establish a rat model of non-alcoholic steatohepatitis (NASH) and investigate the effects of lipid peroxidation, nitric oxide (NO), nitric oxide synthase (NOS) and tumor necrosis factor-α (YNF- The role of cytokines such as growth factor-β (TGF-β) in NASH pathogenesis. Methods Rat NASH model was established by high-fat and high-cholesterol diet for 16 weeks. Serum transaminases, serum and liver MDA, SOD, ), NO, NOS, glutathione (GSH) content. Immunohistochemistry labeled α-SMA, KP-1, TNF-α and TGF-β. Results At the end of the experiment, body weight and liver index in the model group were significantly higher than those in the normal group (P <0.05 and 0.01, respectively). Serum aminotransferase was significantly higher than the normal group (P <0.01). The levels of MDA, SOD, NOS and GSH were not significantly different from those of the normal group (P> 0.05), while the levels of MDA and NO in liver homogenate were significantly higher than those in the normal group (P <0.05 and <0.01, respectively). SOD, NOS and GSH decreased significantly (P <0.05 and 0.01 respectively) compared with the normal group. The expression of α-SMA, KP-1, TNF-α and TGF-β in the model group were significantly higher than those in the normal group (P <0.01). Conclusions Lipid peroxidation injury is enhanced, anti-oxidative ability is reduced, and inflammatory mediators such as TNF-α, TGF-β, NO and other inflammatory mediators are activated and participate in the pathogenesis of NASH, which indicates that NASH can develop liver fibrosis and cirrhosis.