Publication: Anti-apoptotic effects and mechanisms of salvianolic acid A on cardiomyocytes in ischemia-reperfusion injury
Authors
Qian, Wei ; Wang, Zilong ; Xu, Tongda ; Li, Dongye
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
publication.page.editor
publication.page.department
DOI
DOI: 10.14670/HH-18-048
item.page.type
info:eu-repo/semantics/article
Description
Abstract
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 anticancer 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.
publication.page.subject
Citation
Histology and Histopathology, Vol.34, nº3, (2019)
item.page.embargo
Ir a Estadísticas
Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/