3,3′,4,5′-Tetramethoxy-trans-stilbene and 3,4′,5-trimethoxy-trans-stilbene prevent oxygen-glucose deprivation-induced injury in brain endothelial cell

被引:0
|
作者
Zhou, Chunxiu [1 ]
Zhou, Yan [1 ]
Vong, Chi Teng [1 ,2 ]
Khan, Haroon [3 ]
Cheang, Wai San [1 ]
机构
[1] Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Macau, Peoples R China
[2] Univ Macau, Macau Ctr Res & Dev Chinese Med, Macau, Peoples R China
[3] Abdul Wali Khan Univ Mardan, Dept Pharm, Mardan, Pakistan
基金
中国国家自然科学基金;
关键词
blood-brain barrier; ischemic stroke; oxygen-glucose deprivation; resveratrol derivative; tight junction proteins; ISCHEMIC-INJURY; IN-VIVO; STROKE; RESVERATROL; BARRIER; PROTECTS; NEUROPROTECTION; MECHANISMS; KINASE;
D O I
10.1111/jcmm.70008
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Blood-brain barrier (BBB) disruption is a major pathophysiological event of ischemic stroke. Brain microvascular endothelial cells are critical to maintain homeostasis between central nervous system and periphery. Resveratrol protects against ischemic stroke. 3,3 ',4,5 '-tetramethoxy-trans-stilbene (3,3 ',4,5 '-TMS) and 3,4 ',5-trimethoxy-trans-stilbene (3,4 ',5-TMS) are resveratrol derivatives with addition of methoxy groups, showing better pharmacokinetic performance. We aimed to explore their protective effects and underlying mechanisms. Oxygen-glucose deprivation (OGD) model was applied in bEnd.3 cell line, mouse brain microvascular endothelium to mimic ischemia. The cells were pre-treated with 3,3 ',4,5 '-TMS or 3,4 ',5-TMS (1 and 5 mu M, 24 h) and then subjected to 2-h OGD injury. Cell viability, levels of proinflammatory cytokines and reactive oxygen species (ROS), and protein expressions were measured by molecular assays and fluorescence staining. OGD injury triggered cell death, inflammatory responses, ROS production and nuclear factor-kappa B (NF-kappa B) signalling pathway. These impairments were remarkably attenuated by the two stilbenes, 3,3 ',4,5 '-TMS and 3,4 ',5-TMS. They also alleviated endothelial barrier injuries through upregulating the expression of tight junction proteins. Moreover, 3,3 ',4,5 '-TMS and 3,4 ',5-TMS activated 5 ' adenosine monophosphate-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS). Overall, 3,3 ',4,5 '-TMS and 3,4 ',5-TMS exert protective effects against OGD damage through suppressing cell death, inflammatory responses, oxidative stress, as well as BBB disruption on bEnd.3 cells.
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页数:11
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