Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis

doi:10.1007/s11010-016-2868-x

科研成果详情

题名	Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis
作者	Zheng, Xiang-Tao 1; Wu, Zi-Heng 2; Wei, Ye 3; Dai, Ju-Ji 1; Yu, Guan-Feng1; Yuan, FengLai 4; Ye, Le-Chi5
发表日期	2017-01
发表期刊	MOLECULAR AND CELLULAR BIOCHEMISTRY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Autophagy Salidroside Vascular endothelial cells Oxidative stress Signaling pathway
其他关键词	PEROXIDE-INDUCED INJURY ; NF-KAPPA-B ; ISCHEMIA/REPERFUSION INJURY ; DYSFUNCTION ; DEATH ; INHIBITION ; DEFICIENCY ; BIOLOGY ; LIFE
摘要	Vascular endothelial cells are highly sensitive to oxidative stress, and this is one of the mechanisms by which widespread endothelial dysfunction is induced in most cardiovascular diseases and disorders. However, how these cells can survive in oxidative stress environments remains unclear. Salidroside, a traditional Chinese medicine, has been shown to confer vascular protective effects. We aimed to understand the role of autophagy and its regulatory mechanisms by treating human umbilical vein endothelial cells (HUVECs) with salidroside under oxidative stress. HUVECs were treated with salidroside and exposed to hydrogen peroxide (H2O2). The results indicated that salidroside exerted cytoprotective effects in an H2O2-induced HUVEC injury model and suppressed H2O2-induced apoptosis of HUVECs. Pretreatment with 3-methyladenine (3-MA), an autophagy inhibitor, increased oxidative stress-induced HUVEC apoptosis, while the autophagy activator rapamycin induced anti-apoptosis effects in HUVECs. Salidroside increased autophagy and decreased apoptosis of HUVECs in a dose-dependent manner under oxidative stress. Moreover, 3-MA attenuated salidroside-induced HUVEC autophagy and promoted apoptosis, whereas rapamycin had no additional effects compared with salidroside alone. Salidroside upregulated AMPK phosphorylation but downregulated mTOR phosphorylation under oxidative stress; however, administration of compound C, an AMPK inhibitor, abrogated AMPK phosphorylation and increased mTOR phosphorylation and apoptosis compared with salidroside alone. These results suggest that autophagy is a protective mechanism in HUVECs under oxidative stress and that salidroside might promote autophagy through activation of the AMPK pathway and downregulation of mTOR pathway.
资助项目	Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81270011, 81472125]; Zhejiang Provincial Natural Science Foundation of ChinaNatural Science Foundation of Zhejiang Province [LY15H160058]; Zhejiang Provincial Medical technology science [2015KYB245]
出版者	SPRINGER
出版地	DORDRECHT
ISSN	0300-8177
EISSN	1573-4919
卷号	425 期号:1-2 页码:125-138
DOI	10.1007/s11010-016-2868-x
页数	14
WOS类目	Cell Biology
WOS研究方向	Cell Biology
WOS记录号	WOS:000392399700012
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	27848074
SCOPUSEID	2-s2.0-84995494453
通讯作者地址	[Yuan, FengLai]Department of Central Laboratory,The third Hospital Affiliated to Nantong University,Wuxi,214041,China
Scopus学科分类	Molecular Biology;Clinical Biochemistry;Cell Biology
引用统计	被引频次：46[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/9622
专题	附属第一医院_血管外科附属第一医院_肿瘤外科
通讯作者	Yuan, FengLai
作者单位	1.Department of Vascular Surgery,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China; 2.Department of Vascular Surgery,The First Affiliated Hospital,School of Medicine,Zhejiang University,Hangzhou,China; 3.Department of General Surgery,Zhongshan Hospital,Fudan University,Shanghai,China; 4.Department of Central Laboratory,The third Hospital Affiliated to Nantong University,Wuxi,214041,China; 5.Department of Oncological Surgery,The First Affiliated Hospital of Wenzhou Medical University,Nanbaixiang, Ouhai District,Wenzhou,325015,China
第一作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
第一作者的第一单位	附属第一医院
推荐引用方式 GB/T 7714	Zheng, Xiang-Tao,Wu, Zi-Heng,Wei, Ye,et al. Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis[J]. MOLECULAR AND CELLULAR BIOCHEMISTRY,2017,425(1-2):125-138.
APA	Zheng, Xiang-Tao., Wu, Zi-Heng., Wei, Ye., Dai, Ju-Ji., Yu, Guan-Feng., ... & Ye, Le-Chi. (2017). Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis. MOLECULAR AND CELLULAR BIOCHEMISTRY, 425(1-2), 125-138.
MLA	Zheng, Xiang-Tao,et al."Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis".MOLECULAR AND CELLULAR BIOCHEMISTRY 425.1-2(2017):125-138.