Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, PR China.
Biochem Biophys Res Commun. 2013 Nov 15;441(2):351-6. doi: 10.1016/j.bbrc.2013.10.054. Epub 2013 Oct 22.
Oxidative stress is an established event in the pathology of neurobiological diseases. Previous studies indicated that store-operated Ca(2+) entry (SOCE) has been involved in oxidative stress. The present study was carried out to investigate the effects of SOCE inhibition on neuronal oxidative stress injury induced by hydrogen peroxide (H2O2) in HT22 cells, a murine hippocampal neuronal model. H2O2 insult induced significant intracellular Ca(2+) overload, mitochondrial dysfunction and cell viability decrease. Inhibition of SOCE by pharmacological inhibitor and STIM1 RNAi significantly alleviated intracellular Ca(2+) overload, restored the mitochondrial membrane potential (MMP), decreased cytochrome C release and eventually inhibited H2O2-induced cell apoptosis. These findings suggest that SOCE inhibition exhibited neuroprotection against oxidative stress induced by H2O2 and SOCE might be a useful therapeutic target in neurobiological disorders.
氧化应激是神经生物学疾病病理学中的一个既定事件。先前的研究表明，钙库操纵性钙内流（SOCE）参与了氧化应激。本研究旨在探讨 SOCE 抑制对 H2O2 诱导的 HT22 细胞（一种鼠海马神经元模型）神经元氧化应激损伤的影响。H2O2 损伤诱导显著的细胞内 Ca2+超载、线粒体功能障碍和细胞活力下降。通过药理学抑制剂和 STIM1 RNAi 抑制 SOCE 可显著减轻细胞内 Ca2+超载，恢复线粒体膜电位（MMP），减少细胞色素 C 释放，最终抑制 H2O2 诱导的细胞凋亡。这些发现表明，SOCE 抑制对 H2O2 诱导的氧化应激具有神经保护作用，SOCE 可能是神经生物学疾病的一个有用的治疗靶点。
