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 

机构地区：[1]Department of Neurology, People's Hospital of Linyi, Linyi, Shandong Province, China [2]Department of Neurology, People's Hospital of Yishui, Linyi, Shandong Province, China [3]School of Basic Medicine, Taishan Medical University, Taian, Shandong Province, China

出　　处：《Neural Regeneration Research》2018年第8期1433-1439,共7页中国神经再生研究（英文版）

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

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.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.

关 键 词：SELENIUM SELENOCYSTEINE ischemic stroke oxygen glucose deprivation hippocampal neuron MITOCHONDRIA reaction oxygen species superoxide anion oxidative damage APOPTOSIS 

分 类 号：R743[医药卫生—神经病学与精神病学]