Senkyunolide I attenuates oxygen-glucose deprivation/reoxygenation-induced inflammation in microglial cells
Hu, Yang-ye1,2; Wang, Yuan1; Liang, Shuang1; Yu, Xue-li3; Zhang, Lei3; Feng, Lin-yin3; Feng, Yi1
刊名BRAIN RESEARCH
2016-10-15
卷号1649页码:123-131
关键词Senkyunolide I Microglial cells Oxygen-glucose deprivation/reoxygenation TLR4/NF-kappa B pathway HSF-1/Hsp70
ISSN号0006-8993
DOI10.1016/j.brainres.2016.08.012
文献子类Article
英文摘要Over-activated microglia during stroke has been documented to aggravate brain damage. Our previous studies showed that senkyunolide I (SEI) exerted anti-inflammatory effects against endotoxin insult in vitro and ameliorative effects on cerebral ischemia/reperfusion (I/R) injury in vivo. Using oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic stroke, we here investigated the anti-inflammatory effect of SEI on microglial cells and explored the underlying mechanisms. OGD for 3 h followed by reoxygenation for 12 h significantly enhanced the release of pro-inflammatory cytokines and expressions of inflammation-related enzymes in BV-2 cells, which was inhibited by pretreatment with SEI. To elucidate the mechanisms, we studied its effect on upstream signaling pathways. It was found that SEI suppressed the activation of NE-kappa B pathway induced by OGD/R and the MAPK pathway was shown not to be involved. Furthermore, SEI significantly down-regulated TLR4/MyD88 pathway with specifically improving inducible Hsp70 level through increasing HSF-1/DNA binding activity, and these regulations responsive to SEI were attenuated by transfecting Hsp70 siRNA and HSF-1 decoy ODNs. Additionally, SEI exerted similar influence on Hsp70/TLR4/NF-kappa B pathway in rat primary microglial cells. The results suggested that SEI had a potent effect against stroke-induced neuroinflammation through suppressing the TLR4/NE-kappa B pathway by up-regulating Hsp70 dependent on HSF-1. (C) 2016 Elsevier B.V. All rights reserved.
资助项目Chinese Ministry of Education[211060] ; Sci-Tech Innovation Item of Shanghai Education Committee[12ZZ124] ; Research Fund for the Doctoral Program of Higher Education of China[20123107120009]
WOS关键词NECROSIS-FACTOR-ALPHA ; INTERCELLULAR-ADHESION MOLECULE-1 ; FOCAL CEREBRAL-ISCHEMIA ; HEAT-SHOCK PROTEINS ; FACTOR-KAPPA-B ; INNATE IMMUNITY ; ISCHEMIA/REPERFUSION INJURY ; SIGNAL-TRANSDUCTION ; BRAIN-INJURY ; ACTIVATION
WOS研究方向Neurosciences & Neurology
语种英语
出版者ELSEVIER SCIENCE BV
WOS记录号WOS:000386408900013
内容类型期刊论文
源URL[http://119.78.100.183/handle/2S10ELR8/275854]  
专题药理学第二研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Feng, Lin-yin; Feng, Yi
作者单位1.Shanghai Univ Tradit Chinese Med, Engn Res Ctr Modern Preparat TCM, Minist Educ, Shanghai, Peoples R China;
2.Shanghai Univ Tradit Chinese Med, TCM Syndrome & Syst Biol Res Ctr, Shanghai, Peoples R China;
3.Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai, Peoples R China
推荐引用方式
GB/T 7714
Hu, Yang-ye,Wang, Yuan,Liang, Shuang,et al. Senkyunolide I attenuates oxygen-glucose deprivation/reoxygenation-induced inflammation in microglial cells[J]. BRAIN RESEARCH,2016,1649:123-131.
APA Hu, Yang-ye.,Wang, Yuan.,Liang, Shuang.,Yu, Xue-li.,Zhang, Lei.,...&Feng, Yi.(2016).Senkyunolide I attenuates oxygen-glucose deprivation/reoxygenation-induced inflammation in microglial cells.BRAIN RESEARCH,1649,123-131.
MLA Hu, Yang-ye,et al."Senkyunolide I attenuates oxygen-glucose deprivation/reoxygenation-induced inflammation in microglial cells".BRAIN RESEARCH 1649(2016):123-131.
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