Curcumin attenuates left ventricular dysfunction and remodeling in rabbits with chronic heart failure..
- Author:
Yan-Hong TANG
1
;
Ming-Wei BAO
;
Bo YANG
;
Yan ZHANG
;
Bing-Shan ZHANG
;
Qing ZHOU
;
Jin-Ling CHEN
;
Cong-Xin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Curcumin; Heart Failure; drug therapy; Matrix Metalloproteinase 2; metabolism; Matrix Metalloproteinase 9; metabolism; Rabbits; Ventricular Dysfunction, Left
- From: Chinese Journal of Cardiology 2009;37(3):262-267
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Curcumin on rabbits with chronic heart failure.
METHODSHeart failure was induced by combined aortic regurgitation and aortic stenosis in 20 New Zealand rabbits and treated with placebo (HF, n = 10) and Curcumin (Cur, 100 mgxkg(-1)xd(-1), n = 10) for 8 weeks, 10 sham operated rabbits served as controls (Con). Echocardiography was performed in all rabbits at baseline and 8 weeks later. Aortic diameter (AO), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic dimension (LVDs), left ventricular end-diastolic dimension (LVDd), left ventricular posterior wall thickness (LVPW) and interventricular septum thickness (IVS) were measured. Myocardial matrix metalloproteinase (MMP)-2 and MMP-9 expressions and fibrosis were determined by immunohistochemistry and Masson staining respectively.
RESULTSCompared to baseline, LVEF and LVFS were significantly decreased, AO, LVDs, LVDd, LVPW, and IVS significantly increased at 8 weeks after operation in HF group while these changes could be significantly attenuated in Curcumin treated rabbits. The protein expressions of MMP-2 and MMP-9 were significantly down-regulated in HF group and could be significantly up-regulated by Curcumin treatment. The increased collagen deposition in HF group was also significantly reduced by Curcumin treatment.
CONCLUSIONCurcumin attenuated left ventricular dysfunction and remodeling by up-regulating MMPs expressions and reducing myocardial fibrosis.