果糖二磷酸钠镁对心肌细胞缺氧复氧损伤修复作用的体外研究  

Plerosis Effect of Sodium Magnesium Fructose Diphosphate on Hypoxia/ Reoxygenation Injury of My-ocardial Cells in Vitro

作　　者：张成志[1] 周远大[1] 

机构地区：[1]重庆医科大学附属第一医院临床药理研究室,重庆市400016

出　　处：《中国药房》2009年第4期252-253,共2页China Pharmacy

摘　　要：目的:体外研究果糖二磷酸钠镁对缺氧/复氧(H/R)心肌细胞损伤的修复作用及其机制。方法:采用原代培养4d的心肌细胞建立H/R损伤模型,分为H/R组和H/R+果糖二磷酸钠镁高、中、低浓度(4.8、2.4、1.2mg·mL-1)组,另取正常细胞设为正常对照组。加入相应药物处理后分别测定各组细胞中乳酸脱氢酶(LDH)、肌酸激酶(CPK)活性及细胞内游离钙浓度([Ca2+]i),并用透射电镜观察细胞超微结构的变化。结果:与H/R组比较,果糖二磷酸钠镁组能显著降低细胞中LDH、CPK、[Ca2+]i水平(P<0.01或P<0.05),减轻细胞超微结构的损伤。结论:果糖二磷酸钠镁对H/R损伤的心肌细胞具有修复作用,其作用可能与降低钙超载有关,且具有浓度依赖性。OBJECTIVE： To study the plerosis effect of sodium magnesium fructose diphosphate （FDPM） on hypoxia/reoxygenation （H/R） injury of myocardial cells and the possible mechanism. METHODS： The myocardial cells which had been primary cultured for 4 days were used to establish H/R injury model before being assigned to five groups： H/R, H/R ＋ FDPM （4.8, 2.4, 1.2 mg·mL^-1） . Then set up normal control with normal cells. The activities of lactate dehydrogenase（LDH）, creatine phosphokinase （CPK） and the intracellular level of free calcium （[Ca^2＋]i） were detected after being treated with corresponding drugs, and the ultrastructures of myocardial cells were observed under transmission electron microscope. RESULTS： As compared with H/R group, FDPM groups significantly decreased the activities of LDH and CPK and the level of [ Ca^2＋] i （P 〈 0.05 or P 〈 0.01） and relieved the injury of the ultrastructures of myocardial cells. CONCLUSION ： The concentration- dependent plerosis effect of FDPM on H/R injury of myocardial cells might be related to the down-regulation of calcium overload.

关 键 词：果糖二磷酸钠镁 缺氧/复氧损伤 钙超载 超微结构 心肌细胞 

分 类 号：R965[医药卫生—药理学]