Abstract Title:

Curcumin ameliorates left ventricular function in rabbits with pressure overload: inhibition of the remodeling of the left ventricular collagen network associated with suppression of myocardial tumor necrosis factor-alpha and matrix metalloproteinase-2 expression.

Abstract Source:

Biol Pharm Bull. 2004 Feb;27(2):198-202. PMID: 14758033

Abstract Author(s):

Qing-Hai Yao, Dong-Qi Wang, Chang-Cong Cui, Zu-Yi Yuan, Shao-Bo Chen, Xiao-Wei Yao, Jun-Kui Wang, Jiang-Fang Lian

Article Affiliation:

Department of Cardiology, The First Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.


OBJECTIVE: Curcumin is a wide-spectrum cellular protector with antiinflammatory, antioxidizant, and antifibrotic effects. This study was conducted to investigate its effects on myocardial collagen remodeling in pressure overloaded rabbits.

METHODS AND RESULTS: Pressure overloaded rabbits were established by partial abdominal aorta ligation. The rabbits were divided into the sham-operation group, vehicle group and curcumin group. Curcumin was administered orally at a dose of 100 mg/kg.d in 10 ml of 2.5% polyethylene glycol solution and the other 2 groups were given the same dose of polyethylene glycol solution. Compared with the vehicle group, left ventricular function in the curcumin group was significantly ameliorated, as indicated by decreased left ventricular end-diastolic pressure, left ventricle weight to body weight ratio, and the left ventricular posterior wall thickness. The collagen volume fraction in the curcumin group was also reduced. Myocardial tumor necrosis factor (TNF)-alpha and matrix metalloproteinase (MMP)-2 expression were significantly overexpressed in the vehicle group and markedly suppressed in the curcumin group at both the 4th and 8th weeks. At the end of the 8th week, the ejection fraction in the curcumin group was increased compared with that in the vehicle group.

CONCLUSION: Curcumin improved left ventricular function in pressure overloaded rabbits. This might be due to inhibition of collagen remodeling associated with suppression of myocardial expression of tumor necrosis factor-alpha, and matrix metalloproteinase-2.

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