The coordinated effect of the excessive protein and cholesterin intake on inducing rat myocardial fibrosis and its mechanism.
- Author:
Xiao-Hua XIE
1
;
Zhao-Hui LI
;
Wen CHEN
;
Wen-Ning LU
;
Ning LIU
;
Xiu-Hua LIU
;
Chao-Shu TANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cardiomyopathies; etiology; pathology; Cholesterol, Dietary; adverse effects; Dietary Proteins; adverse effects; Fibrosis; Male; Myocardium; pathology; Rats; Rats, Wistar
- From: Chinese Journal of Applied Physiology 2004;20(1):43-45
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the coordinated role and its mechanism of the high protein and hypercholesterol intake on inducing rat myocardial fibrosis.
METHODSThe tissue level of the collagen in left ventricule, the concentrations of the plasma and the cardiac tissue angiotensin II (Ang II) and Aldosterone (Ald), the serum concentration of nitrite (NO2-), in the Wistar rats on diet which adding 20% protein or/and 100 mg/d cholesterin in the rat standard foods for 8 weeks, were measured by the colorimetric analysis of the hydroxyproline, by the radioimmunoassay, and by the assay of Griess, respectively.
RESULTS1.69 times left ventricular collagen contents, 0.7 times plasma concentrations of total cholesterin, 1.5 times levels of the plasma Ang II and 1 time myocardial ald contents were higher, and the serum NO2- concentration was significant lower, in the rats of the high protein and hypercholesterol intake than in the rats of the high protein intake. That 0.48 times left ventricular collagen contents, 0.23 times plasma Ang II in the high protein and hypercholesterol intake rats were higher than in the high cholesterin intake rats.
CONCLUSIONThe excessive protein and cholesterin intake can induce the coordinated effect on developing the myocardial fibrosis of rats. And the mechanism of the fibrosis in rat left ventricule maybe result with the activation of RAAS and the endothelial injury.