阿托伐他汀的新效应：升高心肌细胞载脂蛋白J表达

    New effect of atorvastatin: augmenting ApoJ expression in cardiomyocytes

      摘要
    • 摘要: 目的 观察阿托伐他汀对心肌细胞载脂蛋白(Apo)J的影响。方法 分离大鼠乳鼠心肌细胞，并给予PBS、AngII、阿托伐他汀和ApoJ干预；细胞随机分为对照组； AngII(0.1 μmol/L)组； 阿托伐他汀(10 μmol/L）预处理1h+AngII组； ApoJ(20 μg/ml）预处理1h+AngII组； 通过 MTT检测法和Caspase-3/7活性检测试剂盒检测细胞活性和细胞凋亡变化；利用Western blot检测心肌细胞ApoJ表达情况。结果 与对照组相比，AngII引起心肌细胞活性明显下降(P<0.01)，凋亡细胞显著增加(P<0.01)，心肌细胞ApoJ表达下调(P<0.01)。阿托伐他汀预处理后，再给予AngII干预，与AngII处理组相比，心肌细胞活性明显增加(P<0.01)，凋亡细胞显著减少(P<0.01)，心肌细胞ApoJ表达上调。给予外源性ApoJ预处理，再给予AngII干预，可抑制AngII引起的细胞损伤，作用与阿托伐他汀类似。结论 阿托伐他汀通过升高心肌细胞ApoJ表达，减轻AngII引起的细胞损伤。

       

      Abstract: AIM To investigate whether atorvastatin suppresses cell injury induced by angiotensin II (AngII) via enhancing apolipoprotein J (ApoJ) expression. METHODSCultured neonatal rat ventricular myocytes (NRVMs) were incubated with AngII for 24 h or preincubated with atorvastatin or ApoJ for 1 h. Cell injury was analyzed by MTT and caspase-3/7 assay kits and ApoJ expressions were detected using Western blot analysis. RESULTSAngII significantly increased cell viability and decreased apoptotic cardiomyocytes. ApoJ expression was significantly reduced by AngII. These effects were abolished by atorvastatin. Moreover, ApoJ administration exerted similar effects on NRVMs as atorvastatin. CONCLUSIONAtorvastatin may mediate cardioprotection against cell injury induced by AngII via elevating ApoJ expressions.

       

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