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作 者:沈晓咏[1] 肖明第[1] 杨迪成[1] 林雷[1] 毛建强[1] 胡振雷[1]
机构地区:[1]上海交通大学附属第一人民医院心外科,复旦大学附属华东医院胸外科200080
出 处:《上海医学》2007年第5期354-357,共4页Shanghai Medical Journal
摘 要:目的研究卡维地洛对缺氧/复氧损伤心肌细胞的保护作用,并探讨其可能的作用机制。方法新生1-3 d的Sprague-Dawley鼠,原代分离,培养其心肌细胞72 h后,随机分为正常对照组、单纯缺氧/复氧组及卡维地洛+缺氧/复氧组。先将培养板中的心肌细胞缺氧(氧浓度<1%)120 min,再复氧30 min,造成缺氧/复氧损伤模型,测定细胞存活率;抽取细胞培养上清液测定乳酸脱氢酶(LDH)、磷酸肌酸激酶同工酶(CK-MB);并破碎细胞,测定丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果卡维地洛+缺氧/复氧组的细胞培养液中LDH和CK-MB漏出量分别为(32.32±1.46)和(28.33±2.12)U/L,均显著低于缺氧/复氧组[(50.28±1.22)和(42.45±3.22)U/L,P值均<0.05];卡维地洛+缺氧/复氧组的细胞存活率为(70.21±2.12)%,显著高于缺氧/复氧组[(58.39±3.22)%,P<0.05]。卡维地洛+缺氧/复氧组的细胞内MDA含量为(5.32±0.32)nmol/mL,显著低于缺氧/复氧组[(8.32±0.42)nmol/mL,P<0.05];SOD活性为(10.32±0.42)U/mL,显著高于缺氧/复氧组[(7.42±0.20)U/mL,P<0.05]。结论卡维地洛对心肌细胞缺氧/复氧损伤具有保护作用,能清除氧自由基,提高心肌细胞抗氧化能力。Objective To study the protective effects of carvedilol on neonatal rat cardiomyocyte undergoing hypoxia/reoxygenation injury, and to appraise its possible mechanism. Methods Cardiomyocytes were isolated and purified from neonatal Sprague-Dawley rats cultured for 72 hours and then were divided into three groups: normal control group, simple hypoxia/reoxygenation group, and carvedilol-pretreated group. Hypoxia/reoxygenation model were made by exposing the cardiomyocytes to 120 min of anoxia and 30 min of reoxygenation. The cardiomyocytes viability, lactate dehydrogenase(LDH), isoenzyme of creatine kinase with muscle and brain subunits (CKMB) of the cultured supernatant, and malondialdehyde (MDA), superoxide dismutase (SOD) of cardiomyocytes were all tested. Results The percentage of viable cells, LDH; CK-MB of the cultured supernatant, MDA; SOD of cardiomyocyte of each group were significantly different between one other(P 〈0.05). Conclusion Carvedilol is effective in protecting cardiomyocyte from hypoxia/reoxygenation injury; it can eliminate the free radicals and promote the antioxidization capacity of cardiomyocyte. (Shanghai Med J, 2007, 30 : 354-357)
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