Effect and mechanism of leonurine on pressure overload-induced cardiac hypertrophy in rats.
10.19540/j.cnki.cjcmm.20210805.401
- Author:
Xiao-Li DING
1
;
Qing-Qing YUAN
1
;
Ding-Jia XUE
1
;
Fu-Ming YANG
2
;
Yi-Zhun ZHU
3
;
Hai-Bing QIAN
2
Author Information
1. Guizhou University of Traditional Chinese Medicine Guiyang 550025, China Research Center for Consistency in Property and Effectiveness of Traditional Chinese Medicine, Guizhou University of Traditional Chinese Medicine Guiyang 550025, China.
2. Guizhou University of Traditional Chinese Medicine Guiyang 550025, China.
3. Fudan University Shanghai 201203, China.
- Publication Type:Journal Article
- Keywords:
AT1R;
AngⅡ;
RAS system;
cardiac hypertrophy;
leonurine(Leo)
- MeSH:
Angiotensin II/metabolism*;
Animals;
Cardiomegaly/genetics*;
Gallic Acid/analogs & derivatives*;
Hypertrophy, Left Ventricular/pathology*;
Myocardium/pathology*;
Rats
- From:
China Journal of Chinese Materia Medica
2022;47(2):461-468
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effects of leonurine(Leo) on abdominal aortic constriction(AAC)-induced cardiac hypertrophy in rats and its mechanism. A rat model of pressure overload-induced cardiac hypertrophy was established by AAC method. After 27-d intervention with high-dose(30 mg·kg~(-1)) and low-dose(15 mg·kg~(-1)) Leo or positive control drug losartan(5 mg·kg~(-1)), the cardiac function was evaluated by hemodynamic method, followed by the recording of left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVESP), as well as the maximum rate of increase and decrease in left ventricular pressure(±dp/dt_(max)). The degree of left ventricular hypertrophy was assessed based on heart weight index(HWI) and left ventricular mass index(LVWI). Myocardial tissue changes and the myocardial cell diameter(MD) were measured after hematoxylin-eosin(HE) staining. The contents of angiotensin Ⅱ(AngⅡ) and angiotensin Ⅱ type 1 receptor(AT1 R) in myocardial tissue were detected by ELISA. The level of Ca~(2+) in myocardial tissue was determined by colorimetry. The protein expression levels of phospholipase C(PLC), inositol triphosphate(IP3), AngⅡ, and AT1 R were assayed by Western blot. Real-time quantitative PCR(qRT-PCR) was employed to determine the mRNA expression levels of β-myosin heavy chain(β-MHC), atrial natriuretic factor(ANF), AngⅡ, and AT1 R. Compared with the model group, Leo decreased the LVSP, LVEDP, HWI, LVWI and MD values, but increased ±dp/dt_(max) of the left ventricle. Meanwhile, it improved the pathological morphology of myocardial tissue, reduced cardiac hypertrophy, edema, and inflammatory cell infiltration, decreased the protein expression levels of PLC, IP3, AngⅡ, AT1 R, as well as the mRNA expression levels of β-MHC, ANF, AngⅡ, AT1 R, c-fos, and c-Myc in myocardial tissue. Leo inhibited AAC-induced cardiac hypertrophy possibly by influencing the RAS system.
