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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。
Objective: To investigate the protective effect of “Yinshenkang” on cardiomyocyte hypoxia-reoxygenation injury from the perspective of oxidative stress. Methods: To establish an anoxia / reoxygenation injury model of neonatal rat cardiomyocytes. The serum pharmacology method was used to study the effect of shenshenkang tablet on cell viability. The contents of lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CKMB), superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) were measured. Results: Shenshenkang tablet can obviously improve the myocyte hypoxia-reoxygenation injury myocardial cell activity, and hypoxia injury group A value (0.488 ± 0.023) difference was statistically significant (P <0.05, P <0.01), can reduce LDH , CK, CKMB activity, decreased MDA concentration, increased SOD and GSH activity. CONCLUSION: Inhibition of oxidative stress is one of the mechanisms of Shi Xin Kang Tablet in protecting cardiomyocytes.