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Year : 2018  |  Volume : 13  |  Issue : 8  |  Page : 1433-1439

Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons

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

Correspondence Address:
Xiao-Yan Fu
School of Basic Medicine, Taishan Medical University, Taian, Shandong Province
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Source of Support: The study was supported by the Sci-Tech Development Project of Taian in Shandong, No. 2016NS1058 & 2015NS2081; and the Sci-Tech Development Project of Linyi in Shandong, No. 201515006, Conflict of Interest: None

DOI: 10.4103/1673-5374.235300

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Designing and/or searching for novel antioxidants against oxygen glucose deprivation (OGD)-induced oxidative damage represents an effective strategy for the treatment of human ischemic stroke. Selenium is an essential trace element, which is beneficial in the chemoprevention 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 Na2S4O2, 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 Caspase-7 and Caspase-9 further revealed that OGD-induced apoptosis of HT22 cells was mainly achieved by triggering a mitochondrial-mediated 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.

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