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

• Published in: BMC neuroscience 2017-01, Vol.18 (1), p.15, Article 15
• Main Authors: Ma, Yan-Mei, Ibeanu, Gordon, Wang, Li-Yao, Zhang, Jian-Zhong, Chang, Yue, Dong, Jian-Da, Li, P Andy, Jing, Li
• Format: Article
• Language: English
• Subjects: Animals; Apoptotic Protease-Activating Factor 1 - metabolism; Autophagy - drug effects; Autophagy - physiology; Caspase 3 - metabolism; Caspase 9 - metabolism; Cell death; Cell Line; Cell Survival - drug effects; Cell Survival - physiology; Drug Evaluation, Preclinical; Glutamate; Glutamic Acid - toxicity; Health aspects; Hippocampus (Brain); Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - pathology; Mice; Microtubule-Associated Proteins - metabolism; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria - pathology; Mitochondrial Dynamics - drug effects; Mitochondrial Dynamics - physiology; Neurons; Neuroprotective Agents - pharmacology; Oxidative Stress - drug effects; Oxidative Stress - physiology; Physiological aspects; Selenium (Nutrient); Selenium - pharmacology; Superoxides - metabolism
• ISSN: 1471-2202; 1471-2202
• DOI: 10.1186/s12868-017-0337-4

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. 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. These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.