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首页> 外文期刊>Molecular pharmacology. >Hydrogen sulfide inhibits rotenone-induced apoptosis via preservation of mitochondrial function.
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Hydrogen sulfide inhibits rotenone-induced apoptosis via preservation of mitochondrial function.

机译：硫化氢通过保持线粒体功能来抑制鱼藤酮诱导的细胞凋亡。

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Hydrogen sulfide (H(2)S) has been proposed as a novel neuromodulator, which plays critical roles in the central nervous system affecting both neurons and glial cells. However, its relationship with neurodegenerative diseases is unexplored. The present study was undertaken to investigate the effects of H(2)S on cell injury induced by rotenone, a commonly used toxin in establishing in vivo and in vitro Parkinson's disease (PD) models, in human-derived dopaminergic neuroblastoma cell line (SH-SY5Y). We report here that sodium hydrosulfide (NaHS), an H(2)S donor, concentration-dependently suppressed rotenone-induced cellular injury and apoptotic cell death. NaHS also prevented rotenone-induced p38- and c-Jun NH(2)-terminal kinase (JNK)-mitogen-activated protein kinase (MAPK) phosphorylation and rotenone-mediated changes in Bcl-2/Bax levels, mitochondrial membrane potential (DeltaPsi(m)) dissipation, cytochrome c release, caspase-9/3 activation and poly(ADP-ribose) polymerase cleavage. Furthermore, 5-hydroxydecanoate, a selective blocker of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel, attenuated the protective effects of NaHS against rotenone-induced cell apoptosis. Thus, we demonstrated for the first time that H(2)S inhibited rotenone-induced cell apoptosis via regulation of mitoK(ATP) channel/p38- and JNK-MAPK pathway. Our data suggest that H(2)S may have potential therapeutic value for neurodegenerative diseases, such as PD.
机译：硫化氢（H（2）S）已被提议作为一种新型的神经调节剂，它在影响神经元和神经胶质细胞的中枢神经系统中起关键作用。然而，其与神经退行性疾病的关系尚待探索。进行本研究以研究H（2）S对鱼藤酮诱导的细胞损伤的影响，鱼藤酮是人源性多巴胺能神经母细胞瘤细胞系（SH）在建立体内和体外帕金森氏病（PD）模型中常用的毒素-SY5Y）。我们在这里报告说，硫化氢钠（NaHS），H（2）S供体，浓度依赖性抑制鱼藤酮诱导的细胞损伤和凋亡细胞死亡。 NaHS还可以防止鱼藤酮诱导的p38-和c-Jun NH（2）-末端激酶（JNK）-丝裂原激活的蛋白激酶（MAPK）磷酸化和鱼藤酮介导的Bcl-2 / Bax水平，线粒体膜电位（DeltaPsi （m））耗散，细胞色素c释放，caspase-9 / 3激活和聚（ADP-核糖）聚合酶裂解。此外，5-羟基癸酸酯是线粒体ATP敏感性钾（mitoK（ATP））通道的选择性阻滞剂，减弱了NaHS对鱼藤酮诱导的细胞凋亡的保护作用。因此，我们首次证明了H（2）S通过调节mitoK（ATP）通道/ p38-和JNK-MAPK途径抑制鱼藤酮诱导的细胞凋亡。我们的数据表明H（2）S可能对神经退行性疾病（例如PD）具有潜在的治疗价值。

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