Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis.
Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis.
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亚硒酸钠通过抑制铁死亡促进脊髓损伤后神经功能恢复
DOI：
10.4103/1673-5374.339491
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发表时间：
2022-12
影响因子：
6.1
通讯作者：
Li, Jian-Jun
中科院分区：
文献类型：
--
作者：
Chen, Yi-Xin;Zuliyaer, Talifu;Liu, Bin;Guo, Shuang;Yang, De-Gang;Gao, Feng;Yu, Yan;Yang, Ming-Liang;Du, Liang-Jie;Li, Jian-Jun
关键词：
铁凋亡是近年来发现的一种铁依赖性细胞死亡形式，其发生在各种中枢神经系统疾病或损伤的病理过程中，包括继发性脊髓损伤。硒可抑制脑出血后的铁凋亡，促进神经功能恢复。然而，硒是否能促进脊髓损伤后神经功能的恢复及其机制尚不清楚。在这项研究中，我们在脊髓损伤建模后10分钟将亚硒酸钠（3 μL，2.5 μM）注射到T10脊椎挫伤大鼠模型的损伤部位。我们发现，亚硒酸钠处理大大降低铁浓度和脂质过氧化产物丙二醛和4-羟基壬烯醛的水平。此外，亚硒酸钠还能增加特异性蛋白1和谷胱甘肽过氧化物酶4的蛋白和mRNA表达，促进神经元和少突胶质细胞的存活，抑制星形胶质细胞的增殖，促进脊髓损伤大鼠运动功能的恢复。提示亚硒酸钠可能通过特异性蛋白1/谷胱甘肽过氧化物酶4通路抑制铁凋亡，从而改善脊髓损伤大鼠的运动功能。
Ferroptosis is a recently discovered form of iron-dependent cell death, which occurs during the pathological process of various central nervous system diseases or injuries, including secondary spinal cord injury. Selenium has been shown to promote neurological function recovery after cerebral hemorrhage by inhibiting ferroptosis. However, whether selenium can promote neurological function recovery after spinal cord injury as well as the underlying mechanism remain poorly understood. In this study, we injected sodium selenite (3 µL, 2.5 µM) into the injury site of a rat model of T10 vertebral contusion injury 10 minutes after spinal cord injury modeling. We found that sodium selenite treatment greatly decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal. Furthermore, sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4, promoted the survival of neurons and oligodendrocytes, inhibited the proliferation of astrocytes, and promoted the recovery of locomotive function of rats with spinal cord injury. These findings suggest that sodium selenite can improve the locomotive function of rats with spinal cord injury possibly through the inhibition of ferroptosis via the specificity protein 1/glutathione peroxidase 4 pathway.
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