左卡尼汀抑制过氧化氢介导的NFATc3核转位

 目的:探讨在过氧化氢(H2O2)刺激下，左卡尼汀对心肌细胞内胞浆活化T细胞核因子3（NFATc3）的表达及分布的影响。方法:以200 μmol/L H2O2刺激心肌细胞12 h建立氧化应激模型。在药物处理组，于氧化刺激前30 min加入左卡尼汀及钙调神经磷酸酶（CaN）特异性抑制剂环孢素A(CsA)。待刺激完成后，利用蛋白质免疫印迹法检测细胞内总NFATc3，以及胞浆内和胞核内NFATc3的水平，并以免疫荧光法检测NFATc3在细胞中的分布状况。结果:H2O2刺激不影响心肌细胞NFATc3的表达，但可诱导其由胞浆至胞核的转位。左卡尼汀预处理可以显著抑制NFATc3的核转位。结论: 左卡尼汀可通过抑制NFATc3的核转位发挥其抗氧化应激损伤的作用。

L-Carnitine inhibits H2 O2-mediated NFATc3 nuclear translocation

AIM:To explore the effect of L-carnitine on nuclear factor of activated T-cells,cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation. METHODS:Primary cultured neonatal rat myocardial cells were stimulated by H2O2 at concentration of 200 μmol/L for 12 h to induce oxidative stress injury. In treatment group, L-carnitine and cyclosporin A (CsA), a specific inhibitor of calcineurin (CaN), were administered 30 min prior to H2O2 stimulation. After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting. The method of immunofluoresence was used to evaluate the distribution of NFATc3. RESULTS:H2O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment. CONCLUSION: L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.