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目的探讨甘草酸二铵脂质配位体(DGLL)对非酒精性脂肪肝(NAFLD)大鼠的治疗作用及其相关机制。方法 60只SD大鼠随机分为6组:正常对照组、模型组、DGLL(30、60、120mg/kg)组及阳性对照药联苯双酯(200mg/kg)组,每组10只。采用高脂乳剂灌胃建立大鼠NAFLD模型,并给予DGLL干预,9周后观察大鼠血脂、脂质过氧化水平改变;肝脏免疫组织化学观察NF-κB p65病理变化;Western blotting技术检测肝脏组织NF-κB p65和I-κBα蛋白的表达水平。结果与高脂模型组相比,DGLL能明显降低NAFLD大鼠总胆固醇、甘油三酯、低密度脂蛋白、丙二醛水平,使其高密度脂蛋白、超氧化物歧化酶水平升高;能降低NAFLD大鼠肝脏组织NF-κB p65的表达,下调大鼠肝脏组织NF-κB p65蛋白表达,抑制肝脏组织I-κBα蛋白的降解。结论 DGLL能显著降低高脂饮食诱导的NAFLD大鼠NF-κB p65的水平,该作用与抑制NF-κB p65的表达相关。
Objective To investigate the therapeutic effect and mechanism of DGLL on non-alcoholic fatty liver disease (NAFLD) in rats. Methods Sixty SD rats were randomly divided into six groups: normal control group, model group, DGLL group (30,60,120mg / kg) and positive control group (200mg / kg). The model of NAFLD was established by intragastric administration of high-fat emulsion and the intervention of DGLL was given. After 9 weeks, the levels of lipid and lipid peroxidation were observed. The pathological changes of NF-κB p65 were observed by immunohistochemistry in liver. NF-κB p65 and I-κBα protein expression levels. Results Compared with the model group, DGLL could significantly reduce the level of total cholesterol, triglyceride, low density lipoprotein and malondialdehyde in NAFLD rats, and increase the levels of high density lipoprotein and superoxide dismutase. Reduce the expression of NF-κB p65 in the liver tissue of NAFLD rats, down-regulate the expression of NF-κB p65 protein in the liver and inhibit the degradation of I-κBα protein in the liver. Conclusion DGLL can significantly reduce the level of NF-κB p65 induced by high-fat diet in NAFLD rats, which is related to the inhibition of the expression of NF-κB p65.