胡芦巴碱对缺氧/复氧乳鼠心肌细胞的保护作用

Protective effect of trigonelline on rat cardiomyocytes during hypoxia and reoxygenation

目的探究胡芦巴碱(TRG)对缺氧/复氧乳鼠心肌细胞的保护作用及其机制。方法原代培养SD乳鼠心肌细胞,随机分成3组:正常对照(Control组)、缺氧/复氧组(H/R组)和TRG加缺氧/复氧组(TRG+H/R组);采用流式细胞术分别检测TRG对缺氧/复氧乳鼠心肌细胞凋亡和线粒体膜电位的影响;采用超氧化物歧化酶(SOD)和丙二醛(MDA)试剂盒检测SOD活性和MDA水平,蛋白免疫印迹法(Western blot)检测procaspase-9、cleaved caspase-9、procaspase-3和cleaved caspase-3蛋白水平。结果 TRG能够显著降低缺氧/复氧乳鼠心肌细胞凋亡率(P<0.05),增强SOD活性(P<0.05),减少MDA的生成(P<0.05),稳定线粒体膜电位(P<0.05),促进caspase-9和caspase-3的活化。结论 TRG可减轻缺氧/复氧对乳鼠心肌细胞的损伤,其机制可能与抗脂质过氧化和稳定线粒体膜电位有关。

Objective To investigate the protective effects of trigonelline in neonatal rat cardiomyocytes during hypoxia/ reoxygenatio.n and its mechanism. Methods The neonatal rat cardiomyocytes was randomly divided into the normal control group, the hypoxia/reoxygenation group and the trigonelline group. Flow cytometry was used to determine the apoptosis and mitochondrial membrane potential. The levels of SOD and MDA were measured in different groups. Western blot method was used to measure the procaspase-9,cleaved caspase-9,procaspase-3 and cleaved caspase-3 protein level. Results Trigonelline could inhibit apoptosis （P〈 0.05）, enhanced activity of SOD （P〈0.05）, reduce production of MDA（P〈0.05）, stabilize the mitochondrial membrane potential （P〈0.05） and activate caspase-9 and caspase-3 in neonatal rat cardiomyoeytes during hypoxia/reoxygenation. Conclusion Trigonelline could protect myocardial cells from injury caused by hypoxia and reoxygenation,and the mechanism may be associated with anti-lipid peroxidation and stabilizing mitochondria membrane potential.