期刊
NEUROSCIENCE LETTERS
卷 678, 期 -, 页码 110-117出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2018.05.007
关键词
Ebselen; Mitochondrial; Oxidative stress; Apoptosis; Spinal; Cord injury
资金
- National Natural Science Foundation of China [81771349, 81571209]
- Program for Science &Technology Innovation teams in Universities of Henan Province [18IRTSTHN026]
- Medical Science and Technology Project of Henan Province
- Luoyang Medical and Health Science and Technology Project [1724001A-3]
Ebselen is a fat-soluble small molecule and organic selenium compound that regulates the activity of glutathione peroxidase to alleviate mitochondrial oxidative stress and improve mitochondria] function. In the present study, we aimed to investigate the effects of ebselen on mitochondrial oxidative stress response, mitochondrial apotosis, and motor behaviors after spinal cord injury (SCI). We found that ebselen significantly increased the BBB score in motor behavior, thus suggesting a rescue effect of ebselen on motor function after SCI in rats. Meanwhile, we revealed that ebselen can increase glutathione (GSH) content as well as superoxide dismutase (SOD) and catalase (CAT) activities after SCI-this suggests ebselen has an antioxidant effect. Furthermore, the ATP content and Na+-K+-ATPase activity in mitochondria were increased by ebselen after SCI, while the mitochondrial membrane potential (MMP) was decreased by ebselen. The Cytochrome C and Smac release from mitochondria were reduced by ebselen after SCI, thus indicating improved membrane permeability by ebselen. Moreover, the alterations in caspase-3, Bax and Bcl-2 protein expression, as well as the proportion of cell apoptosis were improved by ebselen treatment, which together suggested that ebselen has an inhibitory effect on mitochondria] apotosis pathways after SCI. Taken together, our results suggest that ebselen can inhibit secondary damage caused by spinal cord injury. Indeed it plays a neuroprotective role in spinal cord injury perhaps by improving mitochondria] function and inhibiting the mitochondria] apoptosis pathway.
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