Inhibition of Heat Shock Protein 90 by 17-AAG Reduces Inflammation via P2X7 Receptor/NLRP3 Inflammasome Pathway and Increases Neurogenesis After Subarachnoid Hemorrhage in Mice.

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作者： Yuchun,Zuo ^[1] ; Jikai,Wang ^[1] ; Fan,Liao ^[1] ; Xiaoxin,Yan ^[2] ; Jianming,Li ^[3] ; Lei,Huang ^[4] ; Fei,Liu ^[5]

作者单位： Department of Neurosurgery, Third XiangYa Hospital, Central South University, Changsha, China. ^[1] Department of Anatomy, XiangYa Medical School, Central South University, Changsha, China. ^[2] Neuroscience Research Center, Changsha Medical University, Changsha, China. ^[3] Department of Physiology and Pharmacology, School of Medicine, Loma Linda University, Loma Linda, CA, United States. ^[4] Department of Neurosurgery, School of Medicine, Loma Linda University, Loma Linda, CA, United States. ^[5]

关键词 17-AAG NLRP3 inflammasome P2X7 receptor heat shock protein 90 neurogenesis purinoceptor subarachnoid hemorrhage

DOI 10.3389/fnmol.2018.00401

PMID 30459553

发布时间 2020-10-01

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Frontiers in molecular neuroscience

2018年11卷

401页

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Inhibition of Heat Shock Protein 90 by 17-AAG Reduces Inflammation via P2X7 Receptor/NLRP3 Inflammasome Pathway and Increases Neurogenesis After Subarachnoid Hemorrhage in Mice.

Frontiers in molecular neuroscience

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Frontiers in molecular neuroscience

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Inhibition of Heat Shock Protein 90 by 17-AAG Reduces Inflammation via P2X7 Receptor/NLRP3 Inflammasome Pathway and Increases Neurogenesis After Subarachnoid Hemorrhage in Mice.

Frontiers in molecular neuroscience

相似文献

Frontiers in molecular neuroscience

相关期刊

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