Effect of crocetin on cardiac hypertrophy induced by overloading pressure in rats.
- Author:
Xiang-chun SHEN
1
;
Zhi-yu QIAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Ca(2+) Mg(2+)-ATPase; metabolism; Cardiomegaly; enzymology; metabolism; Carotenoids; pharmacology; Hydroxyproline; metabolism; Male; Matrix Metalloproteinase 2; metabolism; Matrix Metalloproteinase 9; metabolism; Myocardium; enzymology; Organ Size; drug effects; Rats; Rats, Sprague-Dawley; Sodium-Potassium-Exchanging ATPase; metabolism
- From: Acta Pharmaceutica Sinica 2004;39(3):172-175
- CountryChina
- Language:English
-
Abstract:
AIMTo study the influence of crocetin on cardiac hypertrophy induced by overloading pressure in rats.
METHODSThe model of cardiac hypertrophy was produced by overloading pressure in rats. The animals were divided into five groups: sham-operation group (0.5% CMC-Na, ig), model group (operation + 0.5% CMC-Na, ig), captopril group (operation + 50 mg x kg(-1), ig), crocetin I (100 mg x kg(-1), ig) and crocetin II (50 mg x kg(-1), ig). All animals were treated for 30 d by ig. Then, cardiac indexes were examined. The activity of ATPase and the hydroxyproline content in heart were assayed by colorimetric analysis. Matrix metalloproteinases (MMPs) activity was assayed by SDS-PAGE zymography.
RESULTSCompared with the model group, crocetin was found to significantly reduce the cardiac indexes and the content of hydroxyproline in heart, increase the activity of Na+ , K+ -ATPase, Ca2+, Mg2+ -ATPase and inhibit MMPs activity.
CONCLUSIONThe activity of MMPs may play a key role in the cardiac hypertrophy induced by overloading pressure, and proprably as a result of decreasing the activity of MMPs. Crocetin was shown to prevent remodeling of cardiac hypertrophy induced by overloading pressure.
