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NDT Advance Access originally published online on May 25, 2006
Nephrology Dialysis Transplantation 2006 21(8):2096-2105; doi:10.1093/ndt/gfl194
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Experimental Nephrology

Rosiglitazone ameliorates cisplatin-induced renal injury in mice

Sik Lee1,*, Won Kim1,*, Sang-Ok Moon1, Mi Jeong Sung1, Duk Hoon Kim1, Kyung Pyo Kang1, Yong Bum Jang1, Jung Eun Lee1, Kyu Yun Jang2 and Sung Kwang Park1

1 Department of Internal Medicine and 2 Department of Pathology, Renal Regeneration Laboratory, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Jeonju, Republic of 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, Republic of Korea. Email: parksk{at}chonbuk.ac.kr

Background. Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin nephrotoxicity. Agonists of the peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}), such as rosiglitazone, have been recently demonstrated to regulate inflammation by modulating the production of inflammatory mediators and adhesion molecules. The purpose of this study was to examine the protective effects of rosiglitazone on cisplatin nephrotoxicity and to explore the mechanism of its renoprotection.

Methods. Mice were treated with cisplatin with or without pre-treatment with rosiglitazone. Renal functions, histological findings, aquaporin 2 (AQP2) and adhesion molecule expression, macrophage infiltration and tumour necrosis factor-{alpha} (TNF-{alpha}) levels were investigated. The effect of rosiglitazone on nuclear factor (NF)-{kappa}B activity and on viability was examined using cultured human kidney (HK-2) cells.

Results. Rosiglitazone significantly decreased both the damage to renal function and histological pathology after cisplatin injection. Pre-treatment with rosiglitazone reduced the systemic levels of TNF-{alpha} and down-regulated adhesion molecule expression in addition to the infiltration of inflammatory cells after cisplatin administration. Rosiglitazone restored the decreased AQP2 expression after cisplatin treatment. Pre-treatment with rosiglitazone blocked the phosphorylation of the p65 subunit of NF-{kappa}B in cultured HK-2 cells. Rosiglitazone had a protective effect via a PPAR{gamma}-dependent pathway in cisplatin-treated HK-2 cells.

Conclusion. These results showed that pre-treatment with rosiglitazone attenuates cisplatin-induced renal damage through the suppression of TNF-{alpha} overproduction and NF-{kappa}B activation.

Keywords: cisplatin; nuclear factor-{kappa}B; rosiglitazone; tumour necrosis factor-{alpha}

*The authors wish to be known that, in their opinion, the first two authors contributed equally to this work.


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