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作 者:刘琳[1] 管小琴[1] 王立娟[1] 唐袁婷[1]
机构地区:[1]重庆医科大学分子医学与肿瘤研究中心病理教研室,重庆400016
出 处:《生物医学工程学杂志》2010年第6期1327-1331,共5页Journal of Biomedical Engineering
基 金:重庆市教委科学技术研究资助项目(KJ090327)
摘 要:本实验旨在探讨京尼平和维生素E对非酒精性脂肪肝的作用机理。采用软脂酸诱导L02细胞脂肪变性,建立非酒精性脂肪肝体外模型,用维生素E(VitE)、京尼平及两者合用干预72 h,观察L02细胞脂变程度、线粒体膜电位变化、检测解耦联蛋白2(UCP2)mRNA表达,UCP2、NF-κB和TNF-α蛋白水平表达,以及细胞上清生化水平。结果显示,京尼平和VitE两者合用时肝细胞脂变明显改善,线粒体跨膜电位升高,UCP2的mRNA和UCP2、NF-κB、TNF-α蛋白表达下调(P<0.05),细胞上清中TG、GGT、AST、ALT及MOD含量降低(P<0.05),SOD活力升高(P<0.05)。VitE与京尼平联合应用能显著缓解肝细胞脂肪变性。This study was aimed to detect the effect of genipin and Vitamin E(VitE) on non-alcoholic fatty liver disease.L02 cells were divided into five groups:control group,palmic acid treated group,VitE treated group,genipin treated group,and a combination group.All treatments were terminated at the end of 72 hours.Pathological changes of L02 cells were observed.Mitochondrial membrane potential changes were detected by flow cytometry.MDA,SOD,ALT,AST,GGT,TG in culture medium and expression of UCP2 mRNA and protein in L02 cells were detected.We also studied the effects of genipin and VitE on UCP2 and other related factors such as NF-κB and TNF-α on the L02 cell model of non-alcoholic fatty liver disease.In combination group,the degree of adipose degeneration of L02 cells mitigated significantly;mitochondrial membrane potential and the level of SOD activity increased;the level of MDA,ALT,AST,GGT,TG and the expression of UCP2,NF-κB,TNF-αin L02 cells decreased.The use of genipin in combination with VitE can increase mitochondrial membrane potential and markedly relieve the adipose degeneration of liver cells.
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