Aconitine ameliorates cardiomyocyte hypertrophy induced by angiotensin Ⅱ.
10.19540/j.cnki.cjcmm.20190117.002
- Author:
Ning-Ning WANG
1
;
Jia WANG
1
;
Hong-Ling TAN
2
;
Yu-Guang WANG
2
;
Yue GAO
1
;
Zeng-Chun MA
1
Author Information
1. Guangdong Pharmaceutical University Guangzhou 510006,China Institute of Radiation Medicine,Academy of Military Medical Sciences Beijing 100850,China.
2. Institute of Radiation Medicine,Academy of Military Medical Sciences Beijing 100850,China.
- Publication Type:Journal Article
- Keywords:
H9c2 cells;
aconitine;
angiotensin Ⅱ;
cardiac hypertrophy
- MeSH:
Aconitine;
pharmacology;
Actins;
metabolism;
Angiotensin II;
Atrial Natriuretic Factor;
metabolism;
Cardiac Myosins;
metabolism;
Cardiomegaly;
Cells, Cultured;
Humans;
Hypertrophy;
Myocytes, Cardiac;
drug effects;
Myosin Heavy Chains;
metabolism;
Natriuretic Peptide, Brain;
metabolism
- From:
China Journal of Chinese Materia Medica
2019;44(8):1642-1647
- CountryChina
- Language:Chinese
-
Abstract:
This paper was aimed to investigate the inhibitory effect of aconitine(AC) on angiotensin Ⅱ(Ang Ⅱ)-induced H9 c2 cell hypertrophy and explore its mechanism of action. The model of hypertrophy was induced by Ang Ⅱ(1×10-6 mol·L-1),and cardiomyocytes were incubated with different concentrations of AC. Western blot was used to quantify the protein expression levels of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),β-myosin heavy chain(β-MHC),and α-smooth muscle actin(α-SMA). Real-time quantitative PCR(qRT-PCR) was used to quantify the mRNA expression levels of cardiac hypertrophic markers ANP,BNP and β-MHC. In addition,the fluorescence intensity of the F-actin marker,an important component of myofibrils,was detected by using laser confocal microscope. AC could significantly reverse the increase of total protein content in H9 c2 cells induced by Ang Ⅱ; qRT-PCR results showed that AC could significantly inhibit the ANP,BNP and β-MHC mRNA up-regulation induced by AngⅡ. Western blot results showed that AC could significantly inhibit the ANP,BNP and β-MHC protein up-regulation induced by AngⅡ. In addition,F-actin expression induced by Ang Ⅱ could be inhibited by AC,and multiple indicators of cardiomyocyte hypertrophy induced by Ang Ⅱ could be down-regulated,indicating that AC may inhibit cardiac hypertrophy by inhibiting the expression of hypertrophic factors,providing new clues for exploring the cardiovascular protection of AC.
