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目的探讨马齿苋总黄酮(PTF)对H9c2心肌细胞缺氧/复氧(H/R)损伤的保护作用及可能的作用机制。方法采用培养的H9c2心肌细胞株,分为正常对照组、模型组和PTF 10、30、100 mg.L-1组,建立H/R损伤模型,在H9c2心肌细胞H/R前用PTF预处理12 h,应用MTT比色法检测心肌细胞存活率,测定培养液中肌酸激酶(CK)、乳酸脱氢酶(LDH)释放量,超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果与正常对照组相比,模型组心肌细胞存活数明显减少,心肌细胞培养液中CK和LDH释放量增加(P<0.01),SOD活性下降、MDA含量升高(P<0.01);与模型组相比,PTF 10、30、100 mg.L-1组细胞存活数明显升高,心肌细胞培养液中CK、LDH释放量降低,MDA含量降低,SOD活性增加(P<0.01)。结论 PTF可减轻心肌细胞H/R损伤,具有心肌细胞保护作用,其机制可能与提高SOD活性、增强抗氧化能力有关。
Objective To investigate the protective effect of portulaca total flavone (PTF) on hypoxia / reoxygenation (H / R) injury in H9c2 cardiomyocytes and its possible mechanism. Methods The cultured H9c2 cardiomyocytes were divided into normal control group, untreated group and PTF 10, 30, and 100 mg.L-1 groups. H / R injury model was established and pretreated with PTF before H9c2 cardiomyocytes H / R After 12 h, the survival rate of cardiomyocytes was measured by MTT colorimetric assay. The release of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) )content. Results Compared with the normal control group, the viability of myocardial cells in model group decreased significantly, the release of CK and LDH in myocardial cells increased (P <0.01), the activity of SOD decreased and the content of MDA increased (P <0.01) Compared with the control group, the cell viability in PTF 10, 30, 100 mg.L-1 group was significantly increased, the release of CK and LDH in myocardial cell culture medium was decreased, MDA content was decreased and SOD activity was increased (P <0.01). Conclusions PTF can reduce H / R injury of cardiomyocytes and protect cardiomyocytes. Its mechanism may be related to increasing SOD activity and enhancing antioxidant capacity.