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目的:研究丹参酮ⅡA(tanshinone IIA,Tan)预处理对心肌细胞缺氧/复氧(anoxia/reoxygenation,A/R)损伤的延迟保护作用及其机制。方法:以细胞存活率、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性、丙二醛(MDA)含量及热休克蛋白70(HSP70)蛋白表达等为观察指标,用终浓度分别为2.5,10,40μmol·L-1的Tan预处理原代培养大鼠乳鼠心肌细胞1,24h后观察其对A/R损伤的延迟保护作用及NO合成酶抑制剂L-NAME(0.1mmol·L-1)、丝裂素活化蛋白激酶(MAPKs)抑制剂PD98059(50μmol·L-1)对其延迟保护作用的影响。结果:Tan预处理能显著提高细胞存活率,降低LDH活性,呈剂量依赖性,且显著能增加SOD及GSH-Px活性,降低MDA含量,增加HSP70蛋白表达,能对抗24h后A/R损伤;L-NAME和PD98059能部分取消SF预处理的上述延迟保护作用。结论:Tan预处理对心肌细胞A/R损伤有显著的延迟保护作用,其机制与NO生成、MAPK活化及增加HSP70蛋白表达有关。
Objective: To study the delayed protective effect of tanshinone IIA (Tan) preconditioning on cardiomyocyte anoxia / reoxygenation (A / R) injury and its mechanism. Methods: The cell viability, LDH, GSH-Px activities, malondialdehyde (MDA) content and heat shock protein 70 (HSP70) protein expression were used as observation indexes. Primary cultured rat neonatal rat cardiomyocytes were pretreated with 2.5, 10, 40μmol·L-1 Tan respectively for 1, 24 hours and then observed their effects on A / R injury Delayed protective effect of L-NAME (0.1 mmol·L-1) and PD98059 (50 μmol·L-1), a inhibitor of mitogen-activated protein kinase (MAPK), on the delayed protective effect. Results: Tan pretreatment significantly increased cell viability, decreased LDH activity in a dose - dependent manner, and significantly increased the activities of SOD and GSH-Px, decreased the content of MDA and increased the expression of HSP70, L-NAME and PD98059 partially abolished the above-mentioned delayed protection of SF pretreatment. Conclusion: Tan preconditioning can significantly delay the A / R injury in cardiomyocytes. The mechanism is related to NO production, MAPK activation and HSP70 protein expression.