| First Author | Seno T | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 10 | Pages | e25541 |
| PubMed ID | 22003398 | Mgi Jnum | J:179609 |
| Mgi Id | MGI:5302757 | Doi | 10.1371/journal.pone.0025541 |
| Citation | Seno T, et al. (2011) 15-deoxy-Delta(1)(2),(1) prostaglandin J reduces the formation of atherosclerotic lesions in apolipoprotein E knockout mice. PLoS One 6(10):e25541 |
| abstractText | AIM: 15-deoxy-Delta(1)(2),(1) prostaglandin J (15d-PGJ) is a ligand of peroxisome proliferator-activated receptor gamma (PPARgamma) having diverse effects such as the differentiation of adipocytes and atherosclerotic lesion formation. 15d-PGJ can also regulate the expression of inflammatory mediators on immune cells independent of PPARgamma. We investigated the antiatherogenic effect of 15d-PGJ. METHODS: We fed apolipoprotein (apo) E-deficient female mice a Western-type diet from 8 to 16 wk of age and administered 1 mg/kg/day 15d-PGJ intraperitoneally. We measured atherosclerotic lesions at the aortic root, and examined the expression of macrophage and inflammatory atherosclerotic molecules by immunohistochemical and real-time PCR in the lesion. RESULTS: Atherosclerotic lesion formation was reduced in apo E-null mice treated with 15d-PGJ, as compared to in the controls. Immunohistochemical and real-time PCR analyses showed that the expression of MCP-1, TNF-alpha, and MMP-9 in atherosclerotic lesions was significantly decreased in 15d-PGJ treated mice. The 15d-PGJ also reduced the expression of macrophages and RelA mRNA in atherosclerotic lesions. CONCLUSION: This is the first report 15d-PGJ, a natural PPARgamma agonist, can improve atherosclerotic lesions in vivo. 15d-PGJ may be a beneficial therapeutic agent for atherosclerosis. |
