San-Huang-Xie-Xin-Tang Prevents Rat Hearts from Ischemia/Reperfusion-Induced Apoptosis through eNOS and MAPK Pathways.
San-Huang-Xie-Xin-Tang Prevents Rat Hearts from Ischemia/Reperfusion-Induced Apoptosis through eNOS and MAPK Pathways.
复制标题
San-huang-Xie-XIN-Tang通过ENOS和MAPK途径阻止大鼠心脏缺血/再灌注诱导的凋亡。
DOI：
10.1093/ecam/neq061
复制
发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Yeh JL
中科院分区：
文献类型：
--
作者：
Liou SF;Ke HJ;Hsu JH;Liang JC;Lin HH;Chen IJ;Yeh JL
三黄泻心汤是一种由黄芪、丹参、丹参组成的传统中药。本研究旨在观察SHXT对大鼠急性心肌缺血/再灌注（I/R）诱导的心肌细胞凋亡的保护作用。在I/R（左冠状动脉闭塞45分钟，然后再灌注2小时）之前施用媒介物（静脉内盐水）或SHXT（静脉内或口服）。在溶剂组中，心肌I/R引起心肌梗死，血浆心肌酶升高，严重心律失常和死亡率。DNA梯状条带和Bcl-2/Bax比值显示I/R可诱导心肌细胞凋亡。在SHXT组中，我们发现SHXT显著降低了血浆心肌酶水平，心律失常评分（从5 ± 1降至2 ± 1，P <0.01）和死亡率（从53%降至0%，P <0.01）。此外，与溶剂组相比，静脉注射SHXT预处理可剂量依赖性地减少梗死面积（10 mg kg−1：14.0 ± 0.2 vs 44.5 ± 5.0%，30 mg kg−1：6.2 ± 1.2% vs 44.5 ± 5.0%，均P <0.01）。类似地，口服SHXT剂量依赖性地减少梗死面积。SHXT可明显降低缺血再灌注诱导的细胞凋亡，并增加Bcl-2/Bax比值。最后，我们发现，SHXT抵消I/R诱导的下游信号，导致心肌eNOS表达和血浆亚硝酸盐增加，ERK 1/2，p38和JNK的激活减少。这些数据表明，SHXT对I/R诱导的细胞凋亡具有心脏保护作用，并且这些作用至少部分由eNOS和MAPK通路介导。
San-Huang-Xie-Xin-Tang (SHXT) is a traditional Chinese medication consisting of three herbs, namely Coptidis rhizome, Scutellariae radix and Rhei rhizome. This study aimed to examine the cardioprotective effects of SHXT in a rat model of acute myocardial apoptosis induced by ischemia/reperfusion (I/R). Vehicle (intravenous saline) or SHXT (intravenous or oral) was administered prior to I/R (occlusion of left coronary artery for 45 min followed by reperfusion for 2 h). In the vehicle group, myocardial I/R caused myocardial infarction with increased plasma cardiac enzymes, severe arrhythmia and mortality. Myocardial apoptosis was induced by I/R as evidenced by DNA ladder and Bcl-2/Bax ratio. In the SHXT group, we found that SHXT significantly reduced plasma levels of cardiac enzymes, arrhythmia scores (from 5 ± 1 to 2 ± 1, P < .01) and mortality rate (from 53 to 0%, P < .01). In addition, pretreatment with intravenous SHXT reduced the infarct size dose-dependently when compared with the vehicle group (10 mg kg−1: 14.0 ± 0.2 versus 44.5 ± 5.0%, and 30 mg kg−1: 6.2 ± 1.2% versus 44.5 ± 5.0%, both P < .01). Similarly, oral administration of SHXT reduced the infarct size dose-dependently. Furthermore, SHXT markedly decreased the apoptosis induced by I/R with increased Bcl-2/Bax ratio. Finally, we found that SHXT counteracted the I/R-induced downstream signaling, resulting in increased myocardial eNOS expression and plasma nitrite, and decreased activation of ERK1/2, p38 and JNK. These data suggest that SHXT has cardioprotective effects against I/R-induced apoptosis, and that these effects are mediated, at least in part, by eNOS and MAPK pathways.
登录
查看更多内容
影响因子：
5.7
作者：
CHEN, HC;HSIEH, MT
通讯作者：
HSIEH, MT
影响因子：
3.3
作者：
Huang, Yaw-Bin;Wu, Pao-Chu;Tsai, Yi-Hung
通讯作者：
Tsai, Yi-Hung
影响因子：
6.1
作者：
Liang, Jhy-Chong;Chen, Hen-Rong;Yeh, Jwu-Lai
通讯作者：
Yeh, Jwu-Lai
DOI：
10.1111/j.1440-1681.2007.04814.x
发表时间：
2008-02-01
影响因子：
2.9
作者：
Liu, Yi-Na;Zhou, Zhong-Min;Chen, Peng
通讯作者：
Chen, Peng
影响因子：
5
作者：
Sumeray, MS;Rees, DD;Yellon, DM
通讯作者：
Yellon, DM