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首页> 外文期刊>Biochemistry >Neuroprotection by a-Lipoic Acid in Streptozotocin-Induced Diabetes
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Neuroprotection by a-Lipoic Acid in Streptozotocin-Induced Diabetes

机译：α-硫辛酸在链脲佐菌素诱导的糖尿病中的神经保护作用

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摘要

Glial cells provide structural and metabolic support for neurons,and these cells become reactive to any insult to the central nervous system.The Streptozotocin(STZ)rat model was used to study glial reactivity and the prevention of glio-sis by a-lipoic acid(a-LA)administration.The expression of glial fibrillary acidic protein(GFAP),S100B protein,and neuron specific enolase(NSE)was determined as well as lipid peroxidation(LPO)and glutathione(GSH)levels in some brain tissues.Western blot analyses showed GFAP,S100B,and NSE levels significantly increased under STZ-induced diabetes in brain,and LPO level increased as well.Administration of a-LA reduced the expression both of glial and neuronal markers.In addition,a-LA significantly prevented the increase in LPO levels found in diabetic rats.GSH levels were increased by the administration of a-LA.This study suggests that a-LA prevents neural injury by inhibiting oxidative stress and suppressing reactive gliosis.
机译：胶质细胞为神经元提供结构和代谢支持，这些细胞对中枢神经系统的任​​何损伤都具有反应性。链脲佐菌素（STZ）大鼠模型用于研究神经胶质反应性和α-硫辛酸对神经胶质病的预防作用（测定部分神经胶质纤维酸性蛋白（GFAP），S100B蛋白和神经元特异性烯醇化酶（NSE）的表达以及某些脑组织中脂质过氧化（LPO）和谷胱甘肽（GSH）的水平。分析显示，在STZ诱导的糖尿病中，脑中GFAP，S100B和NSE水平显着升高，LPO水平也升高.a-LA的给药可降低神经胶质和神经元标志物的表达。服用a-LA可增加糖尿病大鼠的LPO水平.GSH含量增加。这项研究表明，a-LA可通过抑制氧化应激和抑制反应性神经胶质增生来预防神经损伤。

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