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丹酚酸 A 对体内和体外心肌缺血再灌注损伤的心脏保护作用。

Cardioprotective effects of salvianolic Acid a on myocardial ischemia-reperfusion injury in vivo and in vitro.

机构信息

School of Pharmacy, Yantai University, Yantai 264005, China.

出版信息

Evid Based Complement Alternat Med. 2012;2012:508938. doi: 10.1155/2012/508938. Epub 2011 Jun 25.

DOI:10.1155/2012/508938
PMID:21789047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3124068/
Abstract

Salvianolic acid A (SAA), one of the major active components of Danshen that is a traditional Chinese medicine, has been reported to possess protective effect in cardiac diseases and antioxidative activity. This study aims to investigate the cardioprotection of SAA in vivo and in vitro using the model of myocardial ischemia-reperfusion in rat and hydrogen peroxide (H(2)O(2))-induced H9c2 rat cardiomyoblasts apoptosis. It was found that SAA significantly limited infarct size of ischemic myocardium when given immediately prior to reperfusion. SAA also significantly suppressed cellular injury and apoptotic cell death. Additionally, the results of western blot and phospho-specific antibody microarray analysis showed that SAA could up-regulate Bcl-2 expression and increase the phosphorylation of proteins such as Akt, p42/p44 extracellular signal-related kinases (Erk1/2), and their related effectors. The phosphorylation of those points was related to suppress apoptosis. In summary, SAA possesses marked protective effect on myocardial ischemia-reperfusion injury, which is related to its ability to reduce myocardial cell apoptosis and damage induced by oxidative stress. The protection is achieved via up-regulation of Bcl-2 expression and affecting protein phosphorylation. These findings indicate that SAA may be of value in cardioprotection during myocardial ischemia-reperfusion injury, which provide pharmacological evidence for clinical application.

摘要

丹酚酸 A（SAA）是一种传统中药丹参的主要活性成分之一，已被报道具有心脏疾病保护作用和抗氧化活性。本研究旨在通过大鼠心肌缺血再灌注模型和过氧化氢（H2O2）诱导的 H9c2 大鼠心肌细胞凋亡模型，体内和体外研究 SAA 的心脏保护作用。结果发现，SAA 在再灌注前即刻给予时可显著限制缺血心肌的梗死面积。SAA 还显著抑制细胞损伤和凋亡细胞死亡。此外，Western blot 和磷酸化特异性抗体微阵列分析的结果表明，SAA 可以上调 Bcl-2 表达并增加 Akt、p42/p44 细胞外信号相关激酶（Erk1/2）及其相关效应物的磷酸化。这些点的磷酸化与抑制细胞凋亡有关。总之，SAA 对心肌缺血再灌注损伤具有显著的保护作用，这与其降低氧化应激诱导的心肌细胞凋亡和损伤的能力有关。这种保护作用是通过上调 Bcl-2 表达和影响蛋白磷酸化来实现的。这些发现表明，SAA 可能在心肌缺血再灌注损伤期间的心脏保护中具有价值，为临床应用提供了药理学证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/ba1d3da18657/ECAM2012-508938.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/fa760b49505d/ECAM2012-508938.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/122e55047253/ECAM2012-508938.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/936b076f847e/ECAM2012-508938.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/b2f04a8999fe/ECAM2012-508938.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/a7ffa623e16a/ECAM2012-508938.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/ba1d3da18657/ECAM2012-508938.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/fa760b49505d/ECAM2012-508938.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/122e55047253/ECAM2012-508938.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/936b076f847e/ECAM2012-508938.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/b2f04a8999fe/ECAM2012-508938.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/a7ffa623e16a/ECAM2012-508938.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/314c/3124068/ba1d3da18657/ECAM2012-508938.006.jpg

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