匹伐他汀和阿托伐他汀诱发HepG2细胞发生胰岛素抵抗

发布时间：2018-07-05 20:28

本文选题：匹伐他汀 + 阿托伐他汀　；参考：《中国药理学与毒理学杂志》2015年01期

【摘要】：目的研究匹伐他汀和阿托伐他汀诱发Hep G2细胞发生胰岛素抵抗的作用。方法 Hep G2细胞分别给予胰岛素0.5μmol·L-1,匹伐他汀1,10和100μmol·L-1,阿托伐他汀1,10和100μmol·L-1,以及阿托伐他汀100μmol·L-1+MK886 100μmol·L-1。48,72和96 h后检测细胞残余[125I]胰岛素结合率,[3H]D-葡萄糖摄取率,糖原和三酰甘油(TG)含量;作用48 h时细胞载脂蛋白A5(Apo A5)mRNA、Apo A5蛋白和Akt信号通路。结果与阴性对照组相比,匹伐他汀和阿托伐他汀对残余[125I]胰岛素结合率和糖原含量无明显作用。阿托伐他汀100μmol·L-1增加TG含量(mg·g蛋白:0.71±0.04 vs 1.51±0.05,P0.05),降低[3H]D-葡萄糖摄取率〔37.2±3.2 vs(26.7±1.9)μmol·g-1·h-1,P0.05),减少磷酸化Akt表达水平(0.92±0.09 vs 0.32±0.02,P0.05),升高Apo A5 mRNA(0.30±0.02 vs 0.69±0.06,P0.05)和蛋白表达水平(0.30±0.04 vs0.91±0.03,P0.05),与胰岛素0.5μmol·L-1组类似。阿托伐他汀100μmol·L-1上述作用与作用时间呈正相关(r=0.729,P0.05),而MK886可拮抗这些作用。结论阿托伐他汀100μmol·L-1时间依赖性地增强Apo A5表达,导致细胞糖脂代谢异常,诱发Hep G2细胞胰岛素抵抗。
[Abstract]:Objective to study the effect of pivastatin and Atto vastatin on insulin resistance in HepG2 cells. Methods HepG2 cells were treated with insulin 0.5 渭 mol L -1, pivastatin 10 and 100 渭 mol L -1, Atto vastatin 10 and 100 渭 mol L -1, and Atto vastatin 100 渭 mol L -1 MK886 100 渭 mol L-1.4872 and 96 h later, the residual [125 I] insulin binding rate, [3H] D-glucose uptake rate, glycogen and triglyceride (TG) levels were measured. Apolipoprotein A5 (Apo A5) mRNAs expressed Apo A5 protein and Akt signaling pathway at 48 h. Results compared with the negative control group, pivastatin and Atto vastatin had no significant effect on the residual insulin binding rate and glycogen content. Atto vastatin 100 渭 mol L ~ (-1) increased TG content (mg g protein: 0.71 卤0.04 vs 1.51 卤0.05), decreased [3H] D- glucose uptake (37.2 卤3.2 vs (26.7 卤1.9) 渭 mol g-1 h-1P 0.05), decreased phosphorylated Akt expression (0.92 卤0.09 vs 0.32 卤0.02p0.05), and increased Apo A5 mRNA and protein expression (0.30 卤0.04 vs0.91 卤0.03P0.05), similar to those in insulin 0.5 渭 mol L-1 group. The above effects of Atto vastatin 100 渭 mol L-1 were positively correlated with the time of action (r 0.729 P 0.05), but MK886 could antagonize these effects. Conclusion Atto vastatin (100 渭 mol L-1) enhances the expression of Apo A5 in a time-dependent manner, leading to abnormal glucose and lipid metabolism and inducing insulin resistance in HepG2 cells.
【作者单位】：中南大学湘雅二医院心血管内科;
【分类号】：R966

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