NaHS restores mitochondrial function and inhibits autophagy by activating the PI3K/Akt/mTOR signalling pathway to improve functional recovery after traumatic brain injury

doi:10.1016/j.cbi.2018.02.028

科研成果详情

题名	NaHS restores mitochondrial function and inhibits autophagy by activating the PI3K/Akt/mTOR signalling pathway to improve functional recovery after traumatic brain injury
作者	Xu, Kebin 1; Wu, Fangfang2; Xu, Ke 3; Li, Zhengmao 1; Wei, Xiaojie4; Lu, Qi1; Jiang, Ting 1; Wu, Fenzan 5; Xu, Xinlong4; Xiao, Jian1; Chen, Daqing2; Zhang, Hongyu1,6
发表日期	2018-04-25
发表期刊	CHEMICO-BIOLOGICAL INTERACTIONS 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Hydrogen sulfide Traumatic brain injury Blood brain barrier Autophagy
其他关键词	HYDROGEN-SULFIDE PROTECTS ; BARRIER INTEGRITY ; CELL-DEATH ; AXON REGENERATION ; DYSFUNCTION ; CARDIOPROTECTION ; NEUROPROTECTION ; DEGENERATION ; CHALLENGES ; APOPTOSIS
摘要	Traumatic brain injury (TBI) is one of the most serious public health problems in the world. TBI causes neurological deficits by triggering secondary injuries. Hydrogen sulfide (H2S), a gaseous mediator, has been reported to exert neuroprotective effects in central nervous system diseases, such as TBI. However, the molecular mechanisms involved in this effect are still unclear. The present study was designed to explore the ability of NaHS, a H2S donor, to provide neuroprotection in a mouse model of TBI and to discover the associated molecular mechanisms of these protective effects. Here, we found that administration of NaHS not only maintained the integrity of the blood brain barrier (BBB), protected neurons from apoptosis, and promoted remyelination and axonal reparation but also protected mitochondrial function. In addition, we found that autophagy was inhibited after treatment with NaHS following TBI, an effect that was induced by activation of the PI3K/AKT/mTOR signalling pathway. Our study indicated that H2S treatment is beneficial for TBI, pointing to H2S as a potential therapeutic target for treating TBI.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81472165, 81772450, 81572237, 81501953]; National Science Fund for Outstanding Young ScholarsNational Natural Science Foundation of China (NSFC)National Science Fund for Distinguished Young Scholars [81722028]; Zhejiang Provincial Natural Science Funding [LQ16H090007]; Traditional Chinese Medicine Health Science and Technology Program of Zhejiang Province [2018ZA117]
出版者	ELSEVIER IRELAND LTD
出版地	CLARE
ISSN	0009-2797
EISSN	1872-7786
卷号	286 页码:96-105
DOI	10.1016/j.cbi.2018.02.028
页数	10
WOS类目	Biochemistry & Molecular Biology ; Pharmacology & Pharmacy ; Toxicology
WOS研究方向	Biochemistry & Molecular Biology ; Pharmacology & Pharmacy ; Toxicology
WOS记录号	WOS:000429592200012
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	29567101
SCOPUSEID	2-s2.0-85044170275
通讯作者地址	[Zhang, Hongyu]Key Laboratory of Biotechnology and Pharmaceutical Engineering,School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,325035,China
Scopus学科分类	Toxicology
引用统计	被引频次：38[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/1818
专题	药学院（分析测试中心）附属第二医院第二临床医学院、附属第二医院、育英儿童医院研究生工作部（研究生院）其他_附属东阳医院（东阳市人民医院）其他_附属慈溪医院（慈溪市人民医院）
通讯作者	Zhang, Hongyu
作者单位	1.Key Laboratory of Biotechnology and Pharmaceutical Engineering,School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,325035,China; 2.Department of Emergency,The Second Affiliated Hospital and Yuying Children's Hospital,Wenzhou Medical University,Wenzhou,325027,China; 3.Institute of Life Sciences,Wenzhou University,Wenzhou,325035,China; 4.Department of Neurosurgery,Cixi People's Hospital,Wenzhou Medical University,Ningbo,315300,China; 5.Science and Education Division,Cixi People's Hospital,Wenzhou Medical University,Ningbo,315300,China; 6.Experimental Research Centre,Dongyang People's Hospital,Wenzhou Medical University,Jinhua,322100,China
第一作者单位	药学院（分析测试中心）
通讯作者单位	药学院（分析测试中心）
第一作者的第一单位	药学院（分析测试中心）
推荐引用方式 GB/T 7714	Xu, Kebin,Wu, Fangfang,Xu, Ke,et al. NaHS restores mitochondrial function and inhibits autophagy by activating the PI3K/Akt/mTOR signalling pathway to improve functional recovery after traumatic brain injury[J]. CHEMICO-BIOLOGICAL INTERACTIONS,2018,286:96-105.
APA	Xu, Kebin., Wu, Fangfang., Xu, Ke., Li, Zhengmao., Wei, Xiaojie., ... & Zhang, Hongyu. (2018). NaHS restores mitochondrial function and inhibits autophagy by activating the PI3K/Akt/mTOR signalling pathway to improve functional recovery after traumatic brain injury. CHEMICO-BIOLOGICAL INTERACTIONS, 286, 96-105.
MLA	Xu, Kebin,et al."NaHS restores mitochondrial function and inhibits autophagy by activating the PI3K/Akt/mTOR signalling pathway to improve functional recovery after traumatic brain injury".CHEMICO-BIOLOGICAL INTERACTIONS 286(2018):96-105.