Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons

作     者：Xian-Jun Wang Mei-Hong Wang Xiao-Ting Fu Ya-Jun Hou Wang Chen Da-Chen Tian Su-Yun Bai Xiao-Yan Fu 

作者机构：Department of Neurology People's Hospital of Linyi Linyi Shandong Province China Department of Neurology People's Hospital of Yishui Linyi Shandong Province China School of Basic Medicine Taishan Medical University Taian Shandong Province China 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2018年第13卷第8期

页      面：1433-1439页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the Sci-Tech Development Project of Taian in Shandong,No.2016NS1058&2015NS2081 the Sci-Tech Development Project of Linyi in Shandong,No.201515006 

主　　题：selenium selenocysteine ischemic stroke oxygen glucose deprivation hippocampal neuron mitochondria reaction oxygen species superoxide anion oxidative damage apoptosis 

摘      要：Designing and/or searching for novel antioxidants against oxygen glucose effective strategy for the treatment of human isdlemic stroke. Selenium is deprivation （OGD）-induced oxidative damage represents an an essential trace dement, which is beneficial in the chemo- prevention and chemotherapy of cerebral ischemic stroke. The underlying mechanisms for its therapeutic effects, however, are not well documented. Selenocysteine （SeC） is a selenium-containing amino acid with neuroprotective potential. Studies have shown that SeC can reduce irradiation-induced DNA apoptosis by reducing DNA damage. In this study, the in vitro protective potential and mechanism of action of SeC against OGD-induced apoptosis and neurotoxicity were evaluated in HT22 mouse hippocampal neurons. We cultured HT22 cells in a glucose-free medium containing 2 mM Na2S402, which formed an OGD environment, for 90 minutes. Findings from MTT, flow cytometry and TUNEL staining showed obvious cytotoxicity and apoptosis in HT22 cells in the OGD condition. The activation of Caspa se-7 and Caspase-9 further revealed that OGD-induced apoptosis of HT22 cells was mainly achieved by triggering a mitochondrial-medi- ated pathway. Moreover, the OGD condition also induced serious DNA damage through the accumulation of reactive oxygen species and superoxide anions. However, SeC pre-treatment for 6 hours effectively inhibited OGD-induced cytotoxicity and apoptosis in HT22 cells by inhibiting reactive oxygen species-mediated oxidative damage. Our findings provide evidence that SeC has the potential to suppress OGD-induced oxidative damage and apoptosis in hippocampal neurons.