2. 您的位置
3. 首页
4. 会议论文
5. Ginkgolide K protects the heart against ER stress injury by activating the IRE1α/XBP1 pathway

Ginkgolide K protects the heart against ER stress injury by activating the IRE1α/XBP1 pathway

来源 :中国药理学会第十四次全国学术大会暨施维雅优秀青年药理学工作者奖20周年学术论坛 | 被引量 : 0次 | 上传用户：Heavenws

【摘 要】

：

OBJECTIVE Here we investigated the effects and the underlying mechanism of Ginkgolide K (1,10-dihydroxy-3, 14-didehydroginkgolide, GK) on cardiac ER stress.

【作 者】

：

WANG Shou-bao WANG Zhen-zhong FAN Qi-ru GUO Jing GINA GA-LI DU Guan-hua WANG Xin XIAO Wei 

【机 构】

：

Faculty of Life Sciences, The University of Manchester, Manchester M13 9NT, UK;Beijing Key Laborator

【出 处】

：

中国药理学会第十四次全国学术大会暨施维雅优秀青年药理学工作者奖20周年学术论坛

【发表日期】

：

2016年11期

【关键词】

：

Ginkgolide K ER stress IRE1α XBP1 ER-associated degradation autophagy 

下载到本地 , 更方便阅读

下载此文 赞助VIP

声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架

论文部分内容阅读

　　OBJECTIVE Here we investigated the effects and the underlying mechanism of Ginkgolide K (1,10-dihydroxy-3, 14-didehydroginkgolide, GK) on cardiac ER stress.

其他文献

Clematichinenoside protects blood brain barrier against ischemic stroke superimposed on systemic inf

Suppression of excessive inflammation can ameliorate blood brain barrier (BBB) injury, which shows therapeutic potential for clinical treatment of brain injury induced by stroke superimposed on system

会议

ClematichinenosideBlood brain barrierSystemic inflammationIschemic strokeZin

DL0805衍生物对肺动脉血管细胞的作用及机制研究

目的:肺动脉高压(Pulmonary artery hypertension,PAH)是以肺动脉压力进行性升高,进而导致右心衰竭为特征的高致死率疾病.目前针对这一疾病已有多种治疗药物应用于临床,但它们主要是通过舒张肺动脉血管来发挥作用,对于肺动脉血管病变未表现出明显治疗作用.因此,目前PAH的治疗药物没有显著提高PAH患者生存率,不能满足临床需求.发现新的、对肺动脉血管病变具有治疗作用的化合物对于

会议

Ginkgolide K protects the heart against ER stress injury by activating the IRE1α/XBP1 pathway

Endoplasmic reticulum (ER) stress is increasingly recognized as an important causal factor of many diseases.Targeting ER stress has now emerged as a new therapeutic strategy for treating cardiovascula

会议

Ginkgolide KER stressIRE1αXBP1ER-associated degradation (ERAD)Autophagy

抗血小板药物靶点P2Y1和P2Y12的信号调节及新药评价

血小板聚集和血栓形成是心脑血管病的主要病因,血小板上有两种主要的ADP受体亚型,即P2Y1和P2Y12.已知P2Y12是抗血小板聚集药物氯毗格雷及类似物的作用靶点,此类药物有很强的抗血小板作用,但容易引起出血的副作用也很明显.因而寻找安全,有效的新型抗血小板药物是心血管药物研发的重要任务.血小板P2Y1受体亚型能否作为抗血小板药物的新靶点仍有待研究.我们借助工具药研究了血小板上这两种受体亚型的信号

会议

Salvianolic acid A attenuates isoproterenol-induced myocardial infarction in mice through PI3K/Akt s

OBJECTIVE To investigate the protective effect of salvianolic acid A (Sal A) on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.

会议

salvianolic acid Aisoproterenolmyocardial infarctionapoptosisinflammationsi

Caffeoylquinic acid derivatives extract of Erigeron multiradiatus alleviated acute myocardial ischem

Erigeron multiradiatus (Lindl.) Benth., has been used in Tibet folk medicine to treat various inflammatory diseases.The aim of this study was to investigate anti-myocardial ischemia and reperfusion (I

会议

Erigeron multiradiatuscaffeoylquinic acidmyocardial Ischemia reperfusioninfla

The role of HSPB1 and ectopic F1Fo-ATPase interaction in hypoxia pulmonary hypertension vascular adv

OBJECTIVE To investigate the role of adventitial vasa vasorum in artery remodeling during the process of pulmonary artery hypertension (PAH) , we checked the small heat shock protein 27/25 (HSPB1) whe

会议

pulmonary hypertensionvascular adventitial remodelingvasa vasorumHSPB1ectopi

Effects of hydrogen-rich saline on platelet activation in hypertensive rats

OBJECTIVE To investigate the effect of hydrogen-rich saline on platelet activation in hypertensive rats.METHODS The male Wistar rats were divided into control group, hypertension group, control + hydr

会议

hypertensionplateletactivationhydrogenoxidative stress

J24924 possesses cardiovascular and renal protective effects on pristane-induced lupus through inhib

OBJECTIVE To explore whether J24924 could prevent the development of pristane-induced lupus in a mouse model, and whether it could protect renal and lower the cardiovascular risk.

会议

J24924SLEmiceROCKskidney and cardiovascular complications

UCN enhances TGF-β-mediated mitoinhibition of VSMCs via counteracting TGF-β-induced cPLA2 expression

OBJECTIVE Urocortins (UCNs) and transforming growth factor-3 (TGF-β) have been demonstrated to participate in various cardiovascular diseases, many of which involve VSMCs proliferation.

会议

urocortinsTGF-betacPLA2vascular smooth muscle cellsmitoinhibition