Thioredoxin-1 Protects Spinal Cord from Demyelination Induced by Methamphetamine through Suppressing Endoplasmic Reticulum Stress and Inflammation.
作者： Lihua Yang , Yinli Guo , Mengbin Huang , Xiaoli Wu , Xiang Li
关键词: Kinase 、 Cell biology 、 Myelin basic protein 、 Chemistry 、 Methamphetamine 、 Unfolded protein response 、 Endoplasmic reticulum 、 Meth- 、 Inflammation 、 Tumor necrosis factor alpha
摘要: Methamphetamine (METH) is a psychostimulant abused around the world. Emerging evidence indicates that METH causes brain damage. However, there are very few reports on METH-induced demyelination. Thioredoxin-1 (Trx-1) redox regulating protein and plays roles in protecting neurons from various stresses. whether Trx-1 resists demyelination induced by has not been reported. In this study, we found thin myelin sheaths spinal cord, whereas overexpression transgenic (TG) mice restored thickness. The expressions of myelin-associated glycoprotein, basic protein, cyclin-dependent kinase 5 were decreased METH, these alterations blocked TG mice. procaspase-12 procaspase-3 expression calpain1 was increased suppressed As same as, extracellular signal-regulated kinase, nuclear factor κB, tumor necrosis factor-alpha, interleukin-1beta which These data suggest may play critical role resisting METH-mediated cord through endoplasmic reticulum stress inflammation pathways.
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