Salvianolic acid B protects cardiomyocytes from angiotensin II-induced hypertrophy via inhibition of PARP-1
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- 作者：Min Liu ; Jiantao Ye ; Si Gao ; Wei Fang ; Hong Li ; Biao Geng ; Jian Zou ; Xi Chen ; Shaorui Chen ; Luankun Zhang ; Zhongbao Yue ; Yunzi Ma ; Hui Gao ; Zhuoming Li ; Peiqing Liu
- 关键词：SalB ; Salvianolic acid B ; 3-AB ; 3-Aminobenzamide ; ANF ; atrial natriuretic factor ; AngII ; Angiotensin II ; BNP ; brain natriuretic polypeptide ; DHE ; dihydroethidium ; MTT ; 3-(4 ; 5)-dimethylthiahiazo(-z-y1)-3 ; 5-di-phenytetrazoliumromide ; NAD ; nicotinamide adenine dinucleotide ; NOX ; NADPH oxidase ; PARP-1 ; poly (ADP-ribose) polymerase-1 ; ROS ; reactive oxygen species
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：14 February, 2014
- 年：2014
- 卷：444
- 期：3
- 页码：346-353
- 全文大小：1475 K
文摘
Salvianolic acid B (SalB), one of the major bioactive components in Salvia miltiorrhiza, has plenty of cardioprotective effects. The present study was designed to investigate the effect of SalB on angiotensin II (AngII)-induced hypertrophy in neonatal rat cardiomyocytes, and to find out whether or not this effect is attributed to inhibition of poly (ADP-ribose) polymerase-1 (PARP-1), which plays a key role in cardiac hypertrophy. Our results showed that SalB prevented the cardiomyocytes from AngII-induced hypertrophy, associated with attenuation of the mRNA expressions of atrial natriuretic factor and brain natriuretic peptide, and reduction in the cell surface area. SalB inhibited the activity of PARP-1. The inhibitory effect was comparable to that of the PARP-1 inhibitor 3-Aminobenzamide (3-AB). In addition, SalB reversed the depletion of cellular NAD+ induced by AngII. Moreover, overexpression of PARP-1 attenuated the anti-hypertrophic effect of SalB. These observations suggested that SalB prevented the cardiomyocytes from AngII-induced hypertrophy, at least partially through inhibition of PARP-1. Moreover, SalB attenuated the generation of oxidative stress via suppression of NADPH oxidase 2 and 4, which might probably contribute to the inhibition of PARP-1. These present findings may shed new light on the understanding of the cardioprotective effect of SalB.