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NDT Advance Access originally published online on March 29, 2005
Nephrology Dialysis Transplantation 2005 20(6):1057-1065; doi:10.1093/ndt/gfh705
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Original Article

Agonist of peroxisome proliferator-activated receptor-{gamma}, rosiglitazone, reduces renal injury and dysfunction in a murine sepsis model

Sik Lee1, Won Kim1, Kyung Pyo Kang1, Sang-ok Moon1, Mi Jeong Sung1, Duk Hoon Kim1, Hyung Jin Kim2 and Sung Kwang Park1

1 Department of Internal Medicine and 2 Urology, Renal Regeneration Laboratory, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Jeonju, South Korea

Correspondence and offprint requests to: Sung Kwang Park, MD, Department of Internal Medicine, Chonbuk National University Medical School, 634-18, Keum-Am Dong, Jeonju, 561-712, South Korea. Email: kidney{at}chonbuk.ac.kr

Background. Agonists of the peroxisome proliferator-activated receptor-{gamma} may help to regulate inflammation by modulating the production of inflammatory mediators and adhesion molecules. The purpose of this study was to determine the protective effects of rosiglitazone on renal injury in a sepsis model and to explore the mechanism.

Methods. In lipopolysaccharide (LPS)-induced mouse sepsis, we examined the effect of rosiglitazone on LPS-induced overproduction of inflammatory mediators, on the expression of adhesion molecules in renal tubular epithelial cells and on renal function. The mechanism of the protective effect was investigated in vitro using human renal tubular epithelial cells.

Results. Rosiglitazone significantly decreased serum tumour necrosis factor (TNF)-{alpha} and interleukin (IL)-1ß levels during sepsis. The levels of blood urea nitrogen and creatinine were significantly lower in mice pre-treated with rosiglitazone than that in LPS-treated mice. Rosiglitazone reduced the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tubular epithelial cells and interstitium of LPS-treated mice. Pre-treatment with rosiglitazone reduced the infiltration of macrophages/monocytes in renal tissue. In cultured tubular epithelial cells, rosiglitazone significantly decreased the expression of ICAM-1 and VCAM-1 induced by TNF-{alpha} or IL-1ß, inhibited the degradation of inhibitor {kappa}B{alpha} (I{kappa}B{alpha}) and blocked the activation of the p65 subunit of nuclear factor (NF)-{kappa}B.

Conclusions. These results indicate that pre-treatment with rosiglitazone attenuated the production of TNF-{alpha} and IL-1ß and reduced adhesion molecule expression in renal tubular epithelial cells of LPS-treated mice. Rosiglitazone has an anti-inflammatory effect in renal tubular epithelial cells through the inhibition of NF-{kappa}B activation.

Keywords: adhesion molecules; renal tubular epithelial cells; rosiglitazone; sepsis


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