AI Article Synopsis
- In the study, researchers analyzed the effects of pioglitazone and rosiglitazone on gene expression and cholesterol accumulation in macrophages, focusing on their roles in preventing artery hardening (atherosclerosis).
- Although pioglitazone was found to be about 10 times less potent than rosiglitazone in activating proatherogenic factors, both drugs similarly enhanced the expression of antiatherogenic factors.
- The findings indicate that, despite pioglitazone's lower potency as a PPARgamma agonist, it plays an equally beneficial role in promoting antiatherogenic effects.
Article Abstract
In order to elucidate the antiatherogenic effects of pioglitazone (a peroxisome proliferator-activated receptor [PPAR]gamma agonist with PPARalpha agonistic activity) and rosiglitazone (a more selective PPARgamma agonist), we examined gene expression and cholesteryl ester accumulation in THP-1-derived macrophages. Pioglitazone enhanced the mRNA expression of the proatherogenic factors CD36 and adipophilin, but was approximately 10 times less potent than rosiglitazone. The potencies of the two agents appeared to correspond to their PPARgamma agonistic activities in this respect. However, both agents were similarly potent in enhancing the mRNA expression of the antiatherogenic factors liver X receptor alpha and ATP-binding cassette-transporter A1. Furthermore, both agents enhanced cholesteryl ester hydrolase mRNA expression and inhibited acyl-CoA cholesterol acyltransferase-1 mRNA expression and cholesteryl ester accumulation in macrophages. In this respect, their potencies appeared to correspond to their PPARalpha agonistic activities. These results suggest that pioglitazone has an equally beneficial effect on antiatherogenic events to rosiglitazone, despite being almost 10 times less potent than a PPARgamma agonist.
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| http://dx.doi.org/10.1016/j.bbrc.2004.08.151 | DOI Listing |
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