Endogenous PPARγ mediates anti-inflammatory activity in murine ischemia-reperfusion injury

被引:230
|
作者
Nakajima, A
Wada, K
Miki, H
Kubota, N
Nakajima, N
Terauchi, Y
Ohnishi, S
Saubermann, LJ
Kadowaki, T
Blumberg, RS
Nagai, R
Matsuhashi, N
机构
[1] Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA USA
[3] Harvard Univ, Sch Med, Ctr Expt Therapeut & Reperfus Injury, Boston, MA USA
[4] Dana Farber Canc Inst, Boston, MA 02115 USA
[5] Med Ctr, Gastroenterol Sect, Boston, MA USA
[6] Univ Tokyo, Dept Gastroenterol, Tokyo, Japan
[7] Univ Tokyo, Dept Metab Dis, Tokyo, Japan
[8] Univ Tokyo, Dept Cardiovasc Dis, Tokyo, Japan
关键词
D O I
10.1053/gast.2001.21191
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor whose activation has been linked to several physiologic pathways including those related to the regulation of intestinal inflammation. We sought to determine whether PPAR gamma could function as an endogenous anti-inflammatory pathway in a murine model of intestinal ischemia-reperfusion (I/R) injury. Methods: PPAR gamma -deficient and wildtype mice were examined for their response to I/R procedure. Treatment with a PPAR gamma -specific ligand was also performed. Results: In a murine model of intestinal I/R injury, we observed more severe injury in PPAR gamma -deficient mice and protection against local and remote tissue injury in mice treated with a PPAR gamma -activating ligand, BRL-49653. Activation of PPAR gamma resulted in down-regulation of intercellular adhesion molecule 1 expression by intestinal endothelium and tissue tumor necrosis factor alpha messenger RNA levels most likely by inhibition of the NF-kappaB pathway. Conclusions: These data strongly suggest that an endogenous PPAR gamma pathway exists in tissues that may be amenable to therapeutic manipulation in I/R-related injuries.
引用
收藏
页码:460 / 469
页数:10
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