L-Carnitine拮抗培养心肌细胞缺氧/复氧损伤

L-Carnitine antagonizes hypoxia/reoxygenation-induced damage in cultured myocardial cells of neonatal rats

目的 探讨L Carnitine对心肌细胞缺氧 /复氧损伤的防护作用及其可能的机制。方法 以原代培养新生鼠心肌细胞建立缺氧 /复氧损伤模型 ,观察不同剂量L Carnitine处理后细胞增殖活性、凋亡细胞百分率及DNA断片化率 ,作为反映L Carnitine对心肌细胞缺氧 /复氧损伤防护作用及其机制的指标。结果 在 5～ 5 0 0 0nmol/L范围内 ,L Carnitine预处理对培养心肌细胞缺氧 /复氧损伤均显示保护效应 ;在 5、5 0及 5 0 0nmol/L时均显著降低DNA断片化率 ;L Carnitine在 5 0nmol/L时与单纯缺氧 /复氧组比较可显著降低凋亡细胞百分率。结论 缺氧 /复氧对心肌细胞的影响之一是可诱导心肌细胞凋亡 ;L Carnitine对培养心肌细胞培养缺氧/复氧损伤具有防护作用 ,其机制可能与抑制缺氧 /复氧诱导细胞凋亡有关。

Objective To explore the protective effects and the possible mechanism of L Carnitine on the primary cultured neonatal rat myocardial cells during hypoxia reoxygenation(H/R). Methods After myocardial cells were isolated from neonatal rats and cultured under hypoxic situation, they were then cultivated with different doses of L Carnitine under hypoxia for various times. Cell proliferation, ratios of DNA fragments and percentages of apoptotic cells were determined to indicate the dose dependent protective effects of L Carnitine and its possible mechanism. Results The L Carnitine between 5～5 000 nmol/L exerted significant protective effects on the primary cultured neonatal myocardial cells during H/R; and 5, 50 and 500 nmol/L of L Carnitine decreased the ratios of DNA fragments markedly compared with control. The addition of 50 nmol/L L Carnitine also leaded to notable reduction of the percentages of apoptotic cells compared with simple H/R treated group. Conclusion H/R can induce the apoptosis of primary cultured myocardial cells of neonatal rats. L Carnitine possesses the protective effects on this injury induced by H/R, probably by the mechanism of its suppressing the apoptosis.