中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Inhibition of stress-activated protein kinase in the ischemic/reperfused heart: role of magnesium tanshinoate B in preventing apoptosis

文献类型:期刊论文

作者Au-Yeung, KKW; Zhu, DY; Karmin, O; Siow, YL
刊名BIOCHEMICAL PHARMACOLOGY
出版日期2001-08-15
卷号62期号:4页码:483-493
关键词apoptosis ischemia protein kinases protein phosphorylation reperfusion
ISSN号0006-2952
DOI10.1016/S0006-2952(01)00686-4
文献子类Article
英文摘要The activation of stress-activated protein (SAP) kinase may lead to an induction of apoptosis that is responsible for part of the cardiomyocyte death in reperfusion injury. The objective of the present study was to investigate the mechanism by which magnesium tanshinoate B (MTB), a bioactive compound isolated from Danshen, prevents apoptosis in cardiomyocytes in the ischemic/reperfused heart. Isolated adult rat hearts were perfused by the Langendorff mode with medium containing MTB prior to the induction of normothermic global ischemia. At the end of the 30-min ischemic period, the heart was reperfused with the same medium with or without MTB for an additional 20 min. In the MTB-treated ischemic/reperfused heart, the number of apoptotic nuclei was reduced by 2.5-fold in comparison to that in untreated ischemic/reperfused controls [23 +/- 4 vs 57 +/- 7 (mean +/- SD) TUNEL-positive cells, respectively, N = 3-4, P < 0.001]. SAP kinase activity was elevated 1.7-fold in ischemic/reperfused rat hearts [35.6 +/- 3.8 vs 21.2 +/- 3.3 (control) (mean +/- SEM) relative densitometric units, N = 4-6, P < 0.05]. Treatment with MTB abolished this elevation in SAP kinase activity (25.0 +/- 5.2 relative densitometric units), which was also decreased by 40% in the nucleus. When the heart was subjected to ischemia alone, there was no significant change in SAP kinase activity in the presence or absence of MTB. MTB did not appear to affect the p38 mitogen-activated protein kinase activity in this model system. In conclusion, MTB was shown to have cardioprotective activity against apoptosis, probably through the inhibition of SAP kinase activity. (C) 2001 Elsevier Science Inc. All rights reserved.
WOS关键词LITHOSPERMIC ACID-B ; SALVIAE-MILTIORRHIZAE-RADIX ; PROGRAMMED CELL-DEATH ; C-JUN ; MYOCARDIAL-ISCHEMIA ; CARDIOMYOCYTE APOPTOSIS ; CARDIOVASCULAR-DISEASE ; CARDIAC MYOCYTES ; RAT-HEART ; IN-VIVO
WOS研究方向Pharmacology & Pharmacy
语种英语
WOS记录号WOS:000169834300012
出版者PERGAMON-ELSEVIER SCIENCE LTD
源URL[http://119.78.100.183/handle/2S10ELR8/274460]  
专题新药研究国家重点实验室
中科院受体结构与功能重点实验室
通讯作者Siow, YL
作者单位1.Univ Hong Kong, Fac Med, Dept Pharmacol, Hong Kong, Hong Kong, Peoples R China
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai, Peoples R China
3.Univ Hong Kong, Fac Med, Sch Tradit Chinese Med, Hong Kong, Hong Kong, Peoples R China
推荐引用方式
GB/T 7714
Au-Yeung, KKW,Zhu, DY,Karmin, O,et al. Inhibition of stress-activated protein kinase in the ischemic/reperfused heart: role of magnesium tanshinoate B in preventing apoptosis[J]. BIOCHEMICAL PHARMACOLOGY,2001,62(4):483-493.
APA Au-Yeung, KKW,Zhu, DY,Karmin, O,&Siow, YL.(2001).Inhibition of stress-activated protein kinase in the ischemic/reperfused heart: role of magnesium tanshinoate B in preventing apoptosis.BIOCHEMICAL PHARMACOLOGY,62(4),483-493.
MLA Au-Yeung, KKW,et al."Inhibition of stress-activated protein kinase in the ischemic/reperfused heart: role of magnesium tanshinoate B in preventing apoptosis".BIOCHEMICAL PHARMACOLOGY 62.4(2001):483-493.

入库方式: OAI收割

来源:上海药物研究所

浏览0
下载0
收藏0
其他版本

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。