Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells.
Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells.
复制标题
硒抑制谷氨酸诱导的细胞死亡并防止海马 HT22 神经元细胞线粒体形态动态改变
DOI：
10.1186/s12868-017-0337-4
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发表时间：
2017-01-19
期刊：
影响因子：
2.4
通讯作者：
Jing L
中科院分区：
文献类型：
--
作者：
Ma YM;Ibeanu G;Wang LY;Zhang JZ;Chang Y;Dong JD;Li PA;Jing L
先前的研究表明，硒补充可能是有益的神经保护对谷氨酸诱导的细胞损伤，其中线粒体功能障碍被认为是一个主要的致病特征。然而，硒保护免受谷氨酸引起的线粒体扰动的确切机制仍然不明确。本研究以谷氨酸暴露的小鼠海马神经元HT 22细胞为模型，探讨硒对线粒体损伤的保护机制。我们发现谷氨酸诱导的细胞毒性与超氧阴离子产生的增加、caspase-9和-3的激活、线粒体分裂标志物的增加以及线粒体形态学的改变有关。硒显着解决谷氨酸诱导的线粒体结构损伤，减轻氧化应激，降低Apaf-1，半胱天冬酶-9和-3的内容，并改变自噬过程中观察到的自噬标记物LC 3-I和LC 3-II的比例下降。这些结果表明，硒对谷氨酸刺激的HT 22细胞损伤的保护作用与改善线粒体动力学失衡有关。
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.