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.
出处
《中国药房》
CAS
CSCD
北大核心
2009年第4期252-253,共2页
China Pharmacy
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
Sodium magnesium fructose diphosphate
Hypoxia reoxygenation injury
Calcium overload
Ultrastructures
Myocardial cell