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目的探讨疏肝健脾方药对非酒精性脂肪性肝病(NAFLD)大鼠肝组织LXRαmRNA及蛋白表达的影响。方法选用SD大鼠55只,随机分为正常组、模型组、疏肝组(灌服3.2 g.kg-1·d-1剂量的柴胡疏肝散)、健脾组(灌服10.0 g.kg-1·d-1剂量的参苓白术散)、综合组(灌服11.9 g.kg-1·d-1剂量的柴胡疏肝散和参苓白术散合方),模型组15只,其余各组10只。采用灌饲高脂肪乳剂(10 ml/kg)的方法复制大鼠NAFLD实验动物模型,给药8 w后处死动物,腹主动脉采血,用全自动生化分析仪检测血脂及肝功;常规HE染色观察肝组织病理变化;RT-PCR方法检测肝组织LXRαmRNA的表达;免疫组织化学方法检测肝组织LXRα蛋白的表达。结果与正常组相比,模型组大鼠肝细胞脂肪变性明显,血脂及肝功均有不同程度的升高(P<0.05,P<0.01),大鼠肝组织LXRαmRNA及蛋白表达明显升高(P<0.01);各给药组血脂及肝功和肝组织LXRαmR-NA及蛋白的表达均较模型组显著降低(P<0.05,P<0.01),其中以健脾组下降最为明显。结论疏肝健脾方药对高脂饮食诱导的大鼠NAFLD有较好的治疗作用,其机制可能与其下调肝脏LXRα的表达有关。
Objective To investigate the effects of Shuganjianpi Decoction on LXRαmRNA and protein expression in liver of non-alcoholic fatty liver disease (NAFLD) rats. Methods Fifty-five SD rats were randomly divided into normal group, model group and Shugan decoction group (given a dosage of 3.2 g · kg-1 · d-1) (P <0.01). The rats in the model group (15 cases) were treated with Shenling Baizhu Powder (with a dose of 1 kg · kg-1 · d-1) Only the rest of the 10 groups. Rat model of NAFLD was injected with high fat emulsion (10 ml / kg). Animals were sacrificed after 8 w and blood was taken from abdominal aorta. Blood lipid and liver function were detected by automatic biochemical analyzer. The pathological changes of liver were observed. The expression of LXRαmRNA in liver tissue was detected by RT-PCR and the expression of LXRα protein in liver tissue was detected by immunohistochemistry. Results Compared with the normal group, the fatty degeneration of hepatic cells in the model group was obvious, the level of lipidemia and liver function were increased to some extent (P <0.05, P <0.01), and the expression of LXRα mRNA and protein in the liver of the model group was significantly increased P <0.01). The expression of LXRαmR-NA and protein in serum, liver and liver of each treatment group were significantly lower than those in model group (P <0.05, P <0.01), especially in spleen group. Conclusion Shuganjianpi Decoction has a good therapeutic effect on NAFLD induced by high-fat diet in rats, which may be related to the down-regulation of LXRα expression in liver.