摘要
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 study therapeutic effects and underlying mechanisms of diammonium glycyrrhizinate lipid ligand （DGLL） on nonalcoholic fatty liver disease （NAFLD）. Methods Sixty SD rats were randomly divided into six groups（10 rats per group）： the model group, 3 DGLL-treated （30, 60, 120mg/kg） groups, the positive control [ treated with biphenyldicarboxylate （200mg/kg） ] group and normal control group. The stomach of the rat of the model group was irrigated with high lipid emulsion. The rats of DGLL groups were irrigated with relative dose of DGLL. After nine weeks, the changes of total cholesterol （TC）, triglyceride （TG）, low density lipoprotein （LDL）, high density lipoprotein （HDL） in serum and the contents of malondialdehyde （MDA）, superoxide dismutase （SOD） in liver homogenate were measured; the NF-KB p65 level in liver tissues was observed by immunohistochemistry, respectively. The expressions of NF-κB p65 and I-κBα in liver were determined by Western blotting. Results Compared with the model group, the levels of TC,TG, LDL, MDA were decreased, meanwhile the activity of HDL and SOD were enhanced, the level of NF-κB in liver tissues was ameliorated remarkably by administration of DGLL. Meanwhile, the up-regulation of NF-κB p65 activity and degradation of I-κBα were reversed by DGLL treatment. Conclusion DGLL ameliorated rat NF-κB expression with NAFLD, which was related to NF-κB p65 down-regulation.
出处
《解剖学报》
CAS
CSCD
北大核心
2011年第6期815-819,共5页
Acta Anatomica Sinica
基金
安徽省教育厅自然科学研究资助项目(KJ2010A183)
