Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

BMC Neuroscience

Research Article

Li Jing¹  Jian-Da Dong¹  Yan-Mei Ma¹  Yue Chang¹  Jian-Zhong Zhang¹  Li-Yao Wang²  P. Andy Li³  Gordon Ibeanu³ 

[1] Department of Pathology, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, 750004, Yinchuan, Ningxia, People’s Republic of China;Department of Pathology, Shanxi Traditional Chinese Medicine Hospital, Xi’an, Shanxi, People’s Republic of China;Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, 27707, Durham, NC, USA;

关键词: Glutamate toxicity;    Autophagy;    Mitochondrial fission;    Selenium;   

DOI  :  10.1186/s12868-017-0337-4

 received in 2016-04-14, accepted in 2017-01-12,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundPrevious studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.ResultsWe find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.ConclusionThese findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.

【 授权许可】

CC BY   
© The Author(s) 2017