从氧化应激角度探讨回心康片心肌保护作用的机制

Investigation of protective mechanism of Huixinkang Tablets on cardiocytes from the perspective of oxidative stress

目的:从氧化应激角度探讨回心康片对心肌细胞缺氧复氧损伤保护作用的机制。方法:建立体外大鼠乳鼠心肌细胞缺氧复氧损伤模型。采用血清药理学方法,研究回心康片对细胞活力的影响;利用全自动生化分析仪测定细胞上清液中乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CKMB)、超氧化歧化酶(SOD)、谷胱甘肽酶(GSH)、丙二醛(MDA)、的含量。结果:回心康片可明显提高缺氧复氧损伤心肌细胞的活力,与缺氧损伤组A值(0.488±0.023)比较差异具有统计学意义(P<0.05,P<0.01);能降低LDH、CK、CKMB活性,降低MDA浓度,提高SOD及GSH活性。结论:抑制氧化应激是回心康片保护心肌细胞的作用机制之一。

To observe the effect of Hui Xin Kang tablets （HXKT） on oxidative stress in cultured hypoxia cardiomyocytes,and explore the mechanism of myocantial protection. Methods： Neonatal cardiomycytes were cultured and cytotoxicity in cultured cardiomyocytes was in- duced by anoxia-reoxia. Then, a method of serum pharmacology was used to study the effect of HXKT on cell viability, which was analyzed using the MTr assay. Super oxide dismutase （SOD）, glutathione（ GSH）, malonaldehyde （MDA） , lactate dehydrogenase （LDH） , creatine kinase （CK） and creatine kinase MB （CKMB） activity in medium were assayed by automatic biochemistry analyzer. Results： The A values indicate that the tablets increase activity of the cells significantly compared with the model group （0. 488± 0. 023） （P 〈 0.05, P 〈 0.01 ）. And it can reduce LDH, CK, CKMB activity and MDA levels and increase SOD and GSH activity in medium. Conclusion： HXKT could in- hibit oxidative stress in myocardial cells, thereby to protect the injuried myocardium.