Sodium pyruvate protects against H2O2 mediated apoptosis in human neuroblastoma cell line-SK-N-MC
Sodium pyruvate protects against H2O2 mediated apoptosis in human neuroblastoma cell line-SK-N-MC
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DOI：
10.1016/s0891-0618(03)00037-1
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发表时间：
2003-10-01
影响因子：
2.8
通讯作者：
Shastry, P
中科院分区：
文献类型：
--
作者：
Jagtap, JC;Chandele, A;Shastry, P
自由基参与了神经元的损伤。本研究旨在探讨自由基清除剂丙酮酸钠对过氧化氢(14202)诱导人神经母细胞瘤细胞株SK-N-MC凋亡的保护作用。在H_2O_2(0.025 mM)作用下，细胞在24 h内出现凋亡，3h后caspase3活性升高，24 h时PARP裂解达到最大，3h后线粒体膜电位开始下降。丙酮酸钠以剂量依赖的方式显著保护细胞(P<；0.05)，染料排斥法检测细胞存活率，TUNEL法检测细胞凋亡率。丙酮酸钠显著抑制caspase3活性、PARP裂解和线粒体膜电位的降低。这些数据表明，丙酮酸钠可以保护过氧化氢引起的神经元损伤。(C)2003爱思唯尔B.V.保留所有权利。
Free radicals are involved in neuronal damage. The present study was aimed to investigate the protective effect of sodium pyruvate-a free radical scavenger against hydrogen peroxide (14202) induced apoptosis in human neuroblastoma cell line-SK-N-MC. On exposure to H2O2 (0.025 mM) cells exhibited apoptosis within 24 h, demonstrating a high caspase 3 activity by 3 h followed by cleavage of PARP that was maximum at 24 h. A break down in the mitochondrial membrane potential was observed 3 h onwards. Sodium pyruvate protected cells significantly (P < 0.05) against apoptosis in a dose dependent manner as assessed for cell viability by dye exclusion method and apoptosis by TUNEL. Sodium pyruvate significantly inhibited caspase 3 activity, cleavage of PARP and breakdown of mitochondrial membrane potential. These data suggest that sodium pyruvate protects neuronal damage caused by H2O2. (C) 2003 Elsevier B.V. All rights reserved.