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目的:观察冠心平对过氧化氢(H2O2)所致乳鼠培养心肌细胞损伤的保护作用。方法:原代培养的新生SD乳大鼠,随机分为正常组、模型组、维拉帕米组、和冠心平3个剂量组。用比色法观察乳鼠心肌细胞培养液的乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)、肌酸激酶(CK)、脂质过氧化产物丙二醛(MDA)的含量及超氧化物歧化酶(SOD)活性,并用光镜观察心肌细胞形态学改变。结果:损伤组乳鼠心肌细胞培养液中LDH、CK-MB、CK和MDA含量非常显著增高,SOD活性非常显著降低(与对照组相比,P<0.01),心肌细胞损伤严重;冠心平保护组与H2O2损伤组相比,LDH、CK-MB、CK和MDA明显降低,SOD活性显著升高(P<0.01,P<0.05),心肌细胞形态学变化减轻。结论:冠心平对H2O2诱导的乳鼠心肌细胞损伤有保护作用,其机制可能与清除氧自由基、抗脂质过氧化损伤有关。
Objective: To observe the protective effect of Guanxinping on hydrogen peroxide (H2O2)-induced neonatal rat cardiomyocyte injury. Methods: Primary cultured newborn SD rats were randomly divided into normal group, model group, verapamil group, and Guanxinping group. Colorimetric method was used to observe lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB), creatine kinase (CK), and lipid peroxidation product malondialdehyde (MDA) in cultured neonatal rat cardiomyocytes. The content and superoxide dismutase (SOD) activity were observed by light microscopy. RESULTS: The contents of LDH, CK-MB, CK and MDA in the cultured neonatal rat cardiomyocytes were significantly increased, SOD activity was significantly decreased (P<0.01 compared with the control group), myocardial cell damage was severe, and the coronary heart was protected. Compared with H2O2 injury group, LDH, CK-MB, CK and MDA were significantly decreased, SOD activity was significantly increased (P<0.01, P<0.05), and the morphological changes of myocardial cells were alleviated. Conclusion: Guanxinping has protective effects on H2O2-induced cardiomyocyte injury in neonatal rats. The mechanism may be related to the clearance of oxygen free radicals and anti-lipid peroxidative damage.