We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells.
- Authors
Yan-Mei Ma; Gordon Ibeanu; Li-Yao Wang; Jian-Zhong Zhang; Yue Chang; Jian-Da Dong; Li, P. Andy; Li Jing; Ma, Yan-Mei; Ibeanu, Gordon; Wang, Li-Yao; Zhang, Jian-Zhong; Chang, Yue; Dong, Jian-Da; Jing, Li
- Abstract
<bold>Background: </bold>Previous 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.<bold>Results: </bold>We 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.<bold>Conclusion: </bold>These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.
- Subjects
SELENIUM; GLUTAMIC acid; OXIDATIVE stress; SUPEROXIDES; CASPASES
- Publication
BMC Neuroscience, 2017, Vol 18, p1
- ISSN
1471-2202
- Publication type
journal article
- DOI
10.1186/s12868-017-0337-4