雷诺嗪对缺氧/复氧诱导H9C2心肌细胞氧化应激损伤的影响

Influence of ranolazine on hypoxia/reoxygenation induced H9C2 cardiomyocyte oxidative stress injury

目的:研究雷诺嗪对缺氧/复氧H9C2心肌细胞氧化应激损伤的影响。方法:通过体外培养心肌H9C2细胞,建立心肌细胞缺氧/复氧模型,实验分为3组:正常对照组(正常培养的心肌H9C2细胞)、缺氧/复氧(H/R)组(H/R模型组),雷诺嗪预处理组(H/R前用15μmol/L的雷诺嗪预处理30min,其他同H/R组)。比较各组心肌细胞存活率、细胞凋亡率、乳酸脱氢酶(LDH)释放量及细胞内丙二醛(MDA)、总超氧化物歧化酶(T-SOD)水平。结果:与正常对照组比较,H/R组H9C2心肌细胞的存活率[(100±00)%比(40.49±0.01)%]、T-SOD[(111.71±0.56)U·mg(prot)^-1比(81.92±1.07)U·mg(prot)^-1]水平显著降低,细胞凋亡率[(2.21±0.07)%比(10.11±0.16)%]、LDH[(825.64±0.01)U/L比(1353.53±0.02)U/L]和MDA[(4.95±0.02)μmol·mg(prot)^-1比(6.65±0.02)μmol·mg(prot)^-1]水平显著增加,P均=0.001;与H/R组比较,雷诺嗪预处理组细胞存活率[(96.82±0.03)%]、T-SOD[(101.86±0.66)U·mg(prot)^-1]水平显著提高,细胞凋亡率[(4.77±0.10)%]、LDH[(1076.76±0.01)U/L]和MDA[(5.24±0.08)μmol·mg(prot)^-1]水平显著降低,P均=0.001。结论:雷诺嗪对缺氧/复氧诱导的H9C2心肌细胞氧化应激的损伤具有保护作用。

Objective:To study influence of ranolazine on hypoxia/reoxygenation(H/R)induced H9C2 cardiomyocyte oxidative stress injury.Methods:Cardiomyocyte H/R model was established via H9C2 cardiomyocyte culture in vitro.They were divided into normal control group(normally cultured H9C2 cardiomyocytes),H/R group(H/R model group)and ranolazine preconditioning group(received 15μmol/L ranolazine preconditioning for 30min before H/R,and the others were same as H/R group).Cardiomyocyte survival rate,apoptosis rate,release amount of lactate dehydrogenase(LDH),levels of intracellular malondialdehyde(MDA)and total superoxide dismutase(T-SOD)were compared among three groups.Results:Compared with normal control group,there were significant reductions in H9C2 cardiomyocyte survival rate[(100±00)%vs.(40.49±0.01)%]and T-SOD level[(111.71±0.56)U·mg(prot)^-1 vs.(81.92±1.07)U·mg(prot)^-1],and significant rise in apoptosis rate[(2.21±0.07)%vs.(10.11±0.16)%],levels of LDH[(825.64±0.01)U/L vs.(1353.53±0.02)U/L]and MDA[(4.95±0.02)μmol·mg(prot)^-1 vs.(6.65±0.02)μmol·mg(prot)^-1]in H/R group,P=0.001 all;compared with H/R group,there were significant rise in H9C2 cardiomyocyte survival rate[(96.82±0.03)%]and T-SOD level[(101.86±0.66)U·mg(prot)^-1],and significant reductions in apoptosis rate[(4.77±0.10)%],levels of LDH[(1076.76±0.01)U/L]and MDA[(5.24±0.08)μmol·mg(prot)^-1]in ranolazine preconditioning group,P=0.001 all.Conclusion:Ranolazine can protect hypoxia/reoxygenation induced H9C2 cardiomyocyte oxidative stress injury.