莱菔硫烷对乳鼠心肌细胞缺血缺氧损伤的保护作用

Protective effects of sulforaphane on cardiomyocyte injury induced by ischemia and hypoxia in neonate rat

目的探讨莱菔硫烷(SFN)对乳鼠心肌细胞缺血缺氧损伤的保护作用及可能机制。方法实验随机分为4组:正常对照组、模型组、SFN低剂量组(10μmol/L)、SFN高剂量组(30μmol/L)。建立心肌细胞缺血缺氧损伤模型,予以SFN干预6h后,AnnexinV荧光染色检测心肌细胞凋亡,酶联免疫吸附测定(ELISA)检测培养液中乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)的含量,蛋白印迹法(Western Blot)检测心肌细胞核因子-κB(NF-κB)水平。结果 SFN减少缺血缺氧心肌细胞的凋亡,减少LDH释放,降低MDA水平,增加SOD水平,心肌细胞NF-κB蛋白表达下降,SFN高剂量组则更明显。结论 SFN对心肌细胞缺血缺氧损伤具有保护作用,作用机制与增强心肌细胞抗氧化能力、抑制NF-κB生成有关。

Objective To explore the protective effects of sulforaphane on myocardial cells injury induced by ischemia-hypoxia in neonatal rat and its possible mechanism. Methods Cultured neonatal rat cardiomyocytes were divided randomly into four groups： control group,model group,low dose of SFN group（10 μmol/L） ,and high dose of SFN group（30μmol/L）. Cardiomyocytes model was established in vitro. After treated with SFN for 6 hours, cardiomyocyte apoptosis was detected by AnnexinV. The contents of LDH, MDA, and SOD were tested by ELISA. The expression of NF-κB protein in cardiomyocytes was determined by Western Blot. Results After treatment by SFN, the apoptosis ceils reduced,the contents of LDH and MDA decreased,and SOD content increased significantly. The level of NF-κB expression decreased, which was more significant in high concentrations. Conclusion SFN can protect myocardial cells from anoxia and ischemic injury,and the mechanism may relate to anti-oxidation effects of SFN and inhibi- tion of NF-κB.