Activation of PPAR-γ by Carbon Monoxide from CORM-2 Leads to the Inhibition of iNOS but not COX-2 Expression in LPS-Stimulated Macrophages

被引：39
作者：
Tsoyi, Konstantin [1 ,2 ]
Ha, Yu Mi [1 ,2 ]
Kim, Young Min [1 ,2 ]
Lee, Young Soo [1 ,2 ]
Kim, Hyo Jung [1 ,2 ]
Kim, Hye Jung [1 ,2 ]
Seo, Han Geuk [1 ,2 ]
Lee, Jae Heun [1 ,2 ]
Chang, Ki Churl [1 ,2 ]
机构：
[1] Gyeongsang Natl Univ, Sch Med, Dept Pharmacol, Biomed Ctr BK21, Jinju 660751, South Korea
[2] Gyeongsang Natl Univ, Biomed Ctr BK21, Inst Life Sci, Jinju 660751, South Korea
来源：
INFLAMMATION | 2009年 / 32卷 / 06期
关键词：
iNOS; COX-2; CORM-2; PPAR-gamma; macrophage; inflammation; NITRIC-OXIDE SYNTHASE; HEME OXYGENASE-1/CARBON MONOXIDE; VASCULAR SMOOTH-MUSCLE; ENDOTHELIAL-CELLS; SCHWANN-CELL; YS; 49; INDUCTION; MOLECULES; LIPOPOLYSACCHARIDE; CO;
D O I：
10.1007/s10753-009-9144-0
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The effect of CO on the expression of iNOS and COX-2 was investigated by using a CO-releasing molecule (CORM)-2 in LPS-activated RAW 264.7 cells in vitro. Interestingly, CORM-2 significantly inhibited iNOS (NO) but not COX-2 (PGE(2)) expression. PPAR-gamma activators such as troglitazone, GW1929, and 15-deoxy-Delta 12, 14- prostaglandin J(2) showed preferential inhibitory effect on iNOS over COX-2 expression in LPS-activated macrophages. The same effect was shown in lung tissues (iNOS, COX-2) and serum (NO, PGE(2)) when administered of CORM-2 in LPS-induced septic mice, indicating that CO derived from CORM-2 differentially regulates iNOS and COX-2 through PPAR-gamma activation under inflammation state.
引用
收藏
页码：364 / 371
页数：8
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