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NDT Advance Access published online on May 27, 2009
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp242
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation

Kyung Pyo Kang1,*, Duk Hoon Kim1,*, Yu Jin Jung1, Ae Sin Lee1, Sik Lee1, Sang Yong Lee2, Kyu Yun Jang3, Mi Jeong Sung4, Sung Kwang Park1 and Won Kim1

1 Department of Internal Medicine and Renal Regeneration Laboratory 2 Department of Radiology 3 Department of Pathology, Research Institute of Clinical Medicine and Diabetic Research Center, Chonbuk National University Medical School, Jeonju 4 Food Function Research Center, Korea Food Research Institute, Seongnam, Gyeongki, Republic of Korea

Correspondence and offprint requests to: Won Kim; E-mail: kwon{at}chonbuk.ac.kr



  Abstract

Background. Cisplatin is a chemotherapeutic agent used in treatment of malignant tumours. However, cisplatin produces various side effects, such as nephrotoxicity, neurotoxicity, emetogenesis and ototoxicity. Inflammation is an important mechanism of cisplatin nephrotoxicity. Alpha-lipoic acid ({alpha}-LA) has anti-inflammatory effects that inhibit both adhesion molecule expression in human endothelial cells and monocyte adhesion by suppressing the nuclear factor-{kappa}B (NF-{kappa}B) signalling pathway. The goals of this study were to investigate the anti-inflammatory effects of {alpha}-LA during cisplatin-induced renal injury and to examine the mechanisms of protection.

Methods. C57BL/6 mice were given cisplatin (20 mg/kg) with or without {alpha}-LA treatment (100 mg/kg for 3 days). Renal function, histological changes, adhesion molecule expression and inflammatory cell infiltration were examined. The effect of {alpha}-LA on NF-{kappa}B activity was evaluated by examining nuclear translocation and phosphorylation of NF-{kappa}B p65 subunits in kidney tissue.

Results. Cisplatin-induced decreases in renal function, measured by blood urea nitrogen, serum creatinine level and renal tubular injury scores, were attenuated by {alpha}-LA treatment. {alpha}-LA decreased the tissue levels of tumour necrosis factor-{alpha}, the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), and suppressed the infiltration of CD11b-positive macrophages. {alpha}-LA also attenuated the cisplatin-induced increases in the phosphorylation and nuclear translocation of NF- {kappa}B p65 subunits in kidney tissue.

Conclusions. These results suggest that {alpha}-LA treatment ameliorates cisplatin-induced acute kidney injury by reducing inflammatory adhesion molecule expression and NF-{kappa}B activity.

Keywords: acute; cisplatin; inflammation; kidney injury; nuclear factor-{kappa}B

* These authors contributed equally to this work.

Received for publication: 15.10.08
Accepted in revised form: 29. 4.09


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