朱肖星, 陈定章, 王文清, 宋宏萍, 冯 桦, 朱妙章, 陈 迈, 周晓东. 吡格列酮通过抑制脂质过氧化减轻内皮素-1引起大鼠心肌细胞的损伤[J]. 心脏杂志, 2015, 27(1): 7-010.
    引用本文: 朱肖星, 陈定章, 王文清, 宋宏萍, 冯 桦, 朱妙章, 陈 迈, 周晓东. 吡格列酮通过抑制脂质过氧化减轻内皮素-1引起大鼠心肌细胞的损伤[J]. 心脏杂志, 2015, 27(1): 7-010.
    shu
    Pioglitazone protects against endothelin-1-induced cardiac myocyte injury through antioxidant potential[J]. Chinese Heart Journal, 2015, 27(1): 7-010.
    Citation: Pioglitazone protects against endothelin-1-induced cardiac myocyte injury through antioxidant potential[J]. Chinese Heart Journal, 2015, 27(1): 7-010.
    shu

    吡格列酮通过抑制脂质过氧化减轻内皮素-1引起大鼠心肌细胞的损伤

    Pioglitazone protects against endothelin-1-induced cardiac myocyte injury through antioxidant potential

      摘要
    • 摘要: 目的:探讨吡格列酮（PIO）减轻内皮素-1（ET-1）引起大鼠心肌细胞损伤的作用及其机制。方法： 将原代培养的大鼠心肌细胞分为5组：DMEM组（对照组）、ET-1组、ET-1+PIO（1×10-9 mol/L） 组、ET-1+PIO（1×10-8 mol/L）组及ET-1+PIO（1×10-7 mol/L）组。将大鼠心肌细胞培养24 h后,吸取培养液，按试剂盒说明书测定心肌细胞培养液中乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）的活性及丙二醛(MDA)的含量。结果： 药物干预24 h，培养液中LDH的活性ET-1组明显高于对照组（P<0.01），而ET-1+PIO组LDH的活性低于ET-1组，其中1×10-8mol/L和1×10-7mol/L PIO+ET-1组较ET-1组明显降低（分别为P<0.05,P<0.01）。SOD的活性：ET-1组明显低于对照组（P<0.01），ET-1+PIO组高于ET-1组，其中1×10-8 mol/L和1×10-7 mol/L PIO+ET-1组较ET-1组明显升高（分别为P<0.05,P<0.01）。MDA的含量：ET-1组明显高于对照组（P<0.01），ET-1+PIO组低于ET-1组，其中1×10-8 mol/L和1×10-7 mol/L PIO+ET-1组较ET-1组明显降低（分别为P<0.05,P<0.01）。结论： PIO可保护ET-1引起损伤的心肌细胞，机制可能与抑制脂质过氧化有关。

       

      Abstract: AIM:To investigate the protective effect of pioglitazone (PIO) against endothelin-1 (ET-1)-induced cardiac myocyte injury and its mechanism. METHODS: Cultured primary cardiac myocytes from neonatal rats were randomly divided into DMEM group (control group), ET-1 group, ET-1+PIO (1×10-9 mol/L) group, ET-1+PIO (1×10-8 mol/L) group and ET-1+PIO (1×10-7 mol/L) group. Using biochemical techniques, supernatants were obtained and tested after 24 h in order to detect levels of LDH, SOD and MDA. RESULTS: At 24 h, LDH level in the ET-1 group was higher than in the control group (P<0.01) and those in the ET-1+PIO groups, especially those in the ET-1+PIO (1×10-8 mol/L) group and ET-1+PIO (1×10-7 mol/L) group (P<0.05 and P<0.01, respectively). SOD activity in the ET-1 group was lower than in the control group (P<0.01). SOD activities in the ET-1+PIO groups were higher than in the ET-1 group. SOD activities in ET-1+PIO (1×10-8 mol/L) group and ET-1+PIO (1×10-7 mol/L) group were significantly higher than in the ET-1 group (P<0.05 and P<0.01, respectively). MDA concentration in the ET-1 group was higher than in the control group (P<0.01). MDA concentrations in the PIO+ET-1 groups were lower than in the ET-1 group. MDA concentrations in the ET-1+PIO (1×10-8 mol/L) group and ET-1+PIO (1×10-7 mol/L) group were significantly lower than in the ET-1 group (P<0.05 and P<0.01, respectively). CONCLUSION: The protective effect of PIO against ET-1-induced cardiac myocyte injury may be related to antioxidant potential.

       

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