【摘要】 目的研究丹参酮Ⅵ(TanshinoneⅥ,Tan)预处理对心肌细胞缺氧/复氧(anoxia/reoxygenation,A/R)损伤的保护作用及其机制。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)活性及丙二醛(MDA)含量等为观察指标,用终浓度分别为0.1、1和10μmol/L的Tan预处理原代培养大鼠乳鼠心肌细胞1h,观察其对A/R损伤的保护作用及NO合成酶抑制剂L-NAME(0.1mmol/L)、K+-ATP通道阻断剂格列苯脲(12μmol/L)对其保护作用的影响。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,能对抗A/R损伤;L-NAME和格列苯脲能部分取消Tan预处理的上述保护作用。结论Tan预处理对心肌细胞A/R损伤有显著的心肌细胞保护作用,其机制可能与NO生成、K+-ATP通道开放有关。更多还原

【Abstract】 Objective To study the cardio protection effects and the mechanism of Tanshinone Ⅵ (Tan) on the primary cultured rat cardiomyocytes subjected to anoxia-reoxygenation (A/R) injury.Methods The primary cultured neonatal rat cardiomyocytes were pretreated with Tan (0.1,1,and 10 μmol/L) or Tan (10 μmol/L) and an inhibitor of nitric oxide synthase,L-NAME (0.1 μmol/L),a potent ATP-sensitive K+ channel blocker,glibenclamide(12 μmol/L),respectively for 1 h,and subjected to A/R injury. Cell viability,the activities of SOD,and GSH-Px,MDA content,and LDH activity in medium were measured.Results Pretreatment with Tan decreased LDH activity and MDA contents,and increased cell viability,SOD,and GSH-Px activities in a concentration dependent manner. The protective effects of Tan were partly abolished by L-NAME or glibenclamide.Conclusion Pre-treatment with TAN before A/R can induce delayed effects by activation of NO and the opening of ATP-sensitive K+channel in rat neonatal cardiomyocytes.更多还原