Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Atorvastatin attenuating down-regulation of peroxisome proliferator-activated receptor gamma in preventing cardiac hypertrophy of rats in vitro and in vivo.

Authors: Ye, P  Sheng, L  Zhang, C  Liu, Y 
Citation: Ye P, etal., J Pharm Pharm Sci. 2006;9(3):365-75.
Pubmed: (View Article at PubMed) PMID:17207419

PURPOSE: To investigate whether the role of atorvastatin in suppression of cardiac hypertrophy is potentially associated with the change of peroxisome proliferator-activated receptor gamma (PPARgamma) expression, and the anti-inflammatory effect in vitro and in vivo. METHOD: Cardiac hypertrophy was established by angiotensin II in neonatal cardiac myocytes in vitro and incomplete ligation of abdominal aorta of SD rats in vivo. PPARgamma and cytokines mRNA expression was evaluated by RT-PCR, and the rate of protein synthesis in cardiac myocytes by 3H-leucine incorporation. RESULTS: Atorvastatin attenuated downregulation of PPARgamma mRNA and inhibited brain natriuretic peptide (BNP), interleukin-1beta (IL-1beta) and matrix metalloproteinase 9 (MMP9) mRNA expression, as well as 3H-leucine incorporation in a dose-dependent manner in vitro. Furthermore, atorvastatin reduced the mRNA expression of BNP, IL-1beta and MMP9, and enhanced PPARgamma mRNA expression, and diminished the pressure overload-induced increase in the ratio of heart weight to body weight, left ventricular wall thickness and myocyte diameter of rats in vivo. CONCLUSION: Atorvastatin prevents cardiac hypertrophy of rats, probably associated with the modulation of PPARgamma and the inhibition of myocardial inflammation. Atorvastatin may play a role in prevention and treatment of cardiovascular diseases characterized by cardiac hypertrophy.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 1642047
Created: 2007-08-29
Species: All species
Last Modified: 2007-08-29
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.