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Anti-apoptotic effects and mechanisms of salvianolic acid A on cardiomyocytes in ischemia-reperfusion injury.
Histology and Histopathology ( IF 2 ) Pub Date : 2018-09-26 , DOI: 10.14670/hh-18-048
Wei Qian 1 , Zilong Wang 2 , Tongda Xu 3 , Dongye Li 1
Affiliation  

Prompt myocardial reperfusion during acute myocardial infarction by fibrinolytic therapy, percutaneous coronary intervention, or coronary artery bypass grafting limits the affected area and improves prognosis. However, reperfusion itself can cause cardiomyocyte damage and decrease treatment efficacy. No treatments that effectively prevent myocardial ischemia/reperfusion (I/R) injury are currently available, and are therefore the focus of ongoing research. Salvianolic acid A (SAA), the active ingredient of the traditional Chinese herbal remedy Salvia miltiorrhiza, has anti-thrombotic activity, anti-inflammatory, and anti-cancer activity; regulates blood lipids and provides hepatic and neural protection. Recent studies demonstrated that SAA inhibits cardiomyocyte apoptosis in response to I/R by the PI3K/Akt, GSK-3β, JNK, and ERK1/2 pathways, and by JNK-ERK1/2 crosstalk. The mechanisms for SAA attenuating cardiomyocytes apoptosis during I/R injury through the P38 MAPK, caspase, JAK/STAT, NF-κB and LOX-1 signaling pathways need further illustration. There may be potential crosstalks between PI3K/Akt and JNK, and Akt/GSK-3β and ERK1/2 in the process of SAA against I/R-incuced cardiomyocytes apoptosis. This review summarizes the recent evidence of the anti-apoptotic effects and mechanisms of SAA against myocardial I/R injury and discusses the basis of potential clinical applications of SAA.

中文翻译:

丹酚酸A对缺血再灌注损伤心肌细胞的抗凋亡作用及其机制。

通过纤溶治疗,经皮冠状动脉介入治疗或冠状动脉搭桥术可以在急性心肌梗塞期间立即进行心肌再灌注,从而限制了患处并改善了预后。但是,再灌注本身会引起心肌细胞损伤并降低治疗效果。目前尚无有效预防心肌缺血/再灌注(I / R)损伤的治疗方法,因此是正在进行研究的重点。丹参酸A(SAA)是中草药丹参中的有效成分,具有抗血栓形成,抗炎和抗癌作用。调节血脂并提供肝和神经保护。最近的研究表明,SAA通过PI3K / Akt,GSK-3β,JNK和ERK1 / 2途径抑制响应I / R的心肌细胞凋亡,并通过JNK-ERK1 / 2串扰。SAA通过P38 MAPK,胱天蛋白酶,JAK / STAT,NF-κB和LOX-1信号通路减弱I / R损伤期间心肌细胞凋亡的机制需要进一步阐明。在SAA对抗I / R引起的心肌细胞凋亡过程中,PI3K / Akt与JNK,Akt /GSK-3β和ERK1 / 2之间可能存在潜在的串扰。这篇综述总结了SAA对心肌I / R损伤的抗凋亡作用和机制的最新证据,并讨论了SAA潜在临床应用的基础。和Akt /GSK-3β和ERK1 / 2在SAA对抗I / R引起的心肌细胞凋亡中的作用。这篇综述总结了SAA对心肌I / R损伤的抗凋亡作用和机制的最新证据,并讨论了SAA潜在临床应用的基础。和Akt /GSK-3β和ERK1 / 2在SAA对抗I / R引起的心肌细胞凋亡中的作用。这篇综述总结了SAA对心肌I / R损伤的抗凋亡作用和机制的最新证据,并讨论了SAA潜在临床应用的基础。
更新日期:2020-08-21
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