RAD001 (everolimus) attenuates experimental autoimmune neuritis by inhibiting the mTOR pathway, elevating Akt activity and polarizing M2 macrophages
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- 作者：Ranran Han1 ; Juan Gao1 ; Hui Zhai ; Jinting Xiao ; Ya'nan Ding ; Junwei Hao ; hjw@tmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：GBS ; Guillain-Barre' syndrome ; EAN ; experimental autoimmune neuritis ; mTOR ; mammalian target of rapamycin ; PNS ; peripheral nervous system ; PBS ; phosphate-buffered saline ; dpi ; days post-immunization ; EMG ; electromyography ; CMAP ; compound muscle action potential ; MNCV ; motor nerve conduction velocity ; MNC ; mononuclear cell ; LFB ; luxol fast blue ; MTS ; 3-(4 ; 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium
- 刊名：Experimental Neurology
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：280
- 期：Complete
- 页码：106-114
- 全文大小：1528 K
文摘
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RAD001 exhibits strong potential as a therapeutic strategy for ameliorating peripheral poly-neuropathy.
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The mechanism underlying the effects of RAD001 in EAN rats involves M2 macrophages polarization.
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RAD001 activates p-Akt via inhibiting mTOR pathway, facilitating the phenotype shift of macrophages to M2 type.