丹参酮ⅡA预处理对大鼠心肌细胞缺氧/复氧损伤的延迟保护作用  

Delayed protection of tanshinone IIA on the primary cultured rat cardiomyocytes subjected to anoxia/reoxygenation injury

作　　者：陈杰[1] 许静[2] 袁芳[1] 元刚[1] 蒋月云[1] 任斌[1] 陈孝[1] 

机构地区：[1]中山大学附属第一医院药学部,广东广州510008 [2]南方医科大学附属华瑞医院药剂科,广东广州510630

出　　处：《中国医院药学杂志》2009年第21期1836-1839,共4页Chinese Journal of Hospital Pharmacy

摘　　要：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 protection effects of tanshinone IIA （Tan）on the primary cultured rat cardio myocytes subjected to anoxia-reoxygenation （A/R） injury. METHODS The primary cultured neonatal rat cardiomyocytes were pretreated with Tan （2. 5 μmol.L^-1 ,10μmol-L ^-1 and 40μmol.^-1 ） or Tan （10 μmol.L^-1 ）and L- NAME（0. 1 mmol-L^-1 ）, PD98059 （50 μmol. L^-1 ） respectively for 1 hour, and subjected to A/R injury after 24 hours. Cell viability, the activities of SOD and GSH-Px, MDA contents, LDH activity in medium and HSP70 protein expression were measured. RESULTS Pretreatment with Tan decreased LDH activity and MDA contents, and increased cell viability, SOD and GSH-Px activities in a concentrationdependent manner,and increased HSP70 protein expression. The delayed protective effects of Tan were partly abolished by L- NAME or PD8059. CONCLUSION Pre-treatment with TAN 24h before ischemia,can induce delayed effects by activation of NO and MAPK signaling pathways and followed increased expression of HSP70 in rat neonatal cardiomyocytes. KEY WORDS：tanshinone IIA; delayed protection; cardiomyocyte

关 键 词：丹参酮ⅡA 延迟保护作用 心肌细胞 

分 类 号：R363[医药卫生—病理学]