Aβ25-35 induce endoplasmic reticulum stress and apoptosis of rat cardiomyocytes
10.3760/cma.j.issn.1008-1372.2015.07.010
- VernacularTitle:Aβ25-35诱导大鼠心肌细胞内质网应激和细胞凋亡的研究
- Author:
Yonghao LU
;
Hengqian ZHANG
;
Hao WU
- Publication Type:Journal Article
- Keywords:
Amyloid beta-protein/PD/AE;
Cardiomyopathies/ET;
Myocytes,cardiac/PA/DE;
Endoplasmic reticulum/DE/ME;
Carrier proteins/DE/ME;
Heat-shock proteins/DE/ME;
Caspase 3/DE/ME;
ADP ribose transferases/DE/ME
- From:
Journal of Chinese Physician
2015;17(7):987-991
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of amyloid-β (Aβ)25-35 on endoplasmic reticulum (ER) stress and apoptosis in cultured rat cardiomocytes,and to elucidate the role of ER stress in the injury of cardiomocytes induced by Aβ25-35.Methods The isolated rat myocardial cells were cultured in vitro.Following stimulation of Aβ25-35 with different dose,the survival ratio was observed with methyl thiazolyl tetrazolium (MTT) method.Hoechst33258 staining was used to observe the morphology of apoptotic changes.The percentage of apoptotic cardiomyocytes was quantified with flow cytometry.The expressions of ER stree proteins,including X box-binding protein-1 (XBP-1),glucose-regulated protein 78 (GRP78),and CCAAT/enhancer-binding protein homologous protein (CHOP) were measured with Western blot.The cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP) were measured with Western blot.Results Aβ25-35 decreased the survival ratio and induced the apoptosis of cultured rat cardiomocytes in dose-dependent mode.Meanwhile,Aβ25-35 increased the expressions of ER stree proteins,including XBP-1,GRP78,and CHOP.Aβ25-35 increased the expressions of cleaved caspase-3 and cleaved PARP.Conclusions Aβ25-35 could induce the apoptosis of rat cardiomyocytes,which were involved in ER stress possibly.This study might provide a new strategy for clinical treatment of Alzheimer's disease (AD)-associated myocardial injury.
