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目的通过高脂喂养建立非酒精性脂肪肝病(NAFLD)模型,检测肝组织中丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)及肝脏核因子(NF)-κB p65的表达,探讨NAFLD的发病机制。方法将24只雄性SD大鼠随机分为模型组和正常对照组,每组12只,模型组给予高脂喂养,正常对照组给予普通喂养,第12周末处死大鼠。每周测各组大鼠体质量,比较2组肝组织匀浆中MDA、TNF-α的水平、肝脏组织病理改变程度及NF-κB p65的表达水平。结果模型组体质量和肝指数高于正常对照组(P<0.05)。模型组肝匀浆MDA、TNF-α水平及组织病变程度均高于正常对照组(P<0.05)。模型组肝细胞NF-κB p65表达阳性率和阳性率评分均显著高于正常对照组(P<0.05)。结论NAFLD的肝脏氧化应激较正常增加,且NF-κB p65表达增加,氧化应激可能通过NF-κB通路参与NAFLD疾病的发展。
Objective To establish a non-alcoholic fatty liver disease (NAFLD) model by high fat diet to detect the expression of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and hepatic nuclear factor (NF) To investigate the pathogenesis of NAFLD. Methods Twenty-four male Sprague-Dawley rats were randomly divided into model group and normal control group, with 12 rats in each group. The model group was fed with high fat diet. The normal control group was given normal feeding and the rats were sacrificed at the end of the 12th week. The body weight of rats in each group was measured weekly. The levels of MDA and TNF-α, the histopathological changes of liver tissue and the expression of NF-κB p65 in the two groups of liver homogenates were compared. Results The body weight and liver index of the model group were higher than those of the normal control group (P <0.05). The level of MDA, TNF-α in liver homogenate and the degree of tissue lesion in model group were higher than those in normal control group (P <0.05). The positive expression rate and positive rate of NF-κB p65 in model group were significantly higher than those in normal control group (P <0.05). Conclusion NAFLD liver oxidative stress than normal, and NF-κB p65 expression increased, and oxidative stress may be involved in the development of NAFLD disease through NF-κB pathway.