1. ¹Food Function Research Center, Korea Food Research Institute, Seongnam, Gyeongki, Republic of Korea
2. ²Renal Regeneration Laboratory, Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Jeonju, Republic of Korea

Correspondence: Dae Young Kwon, Korea Food Research Institute, Food Function Research Center, 516, Baekhyun-Dong, Bundang-Ku, Songnam, Gyeongki 463-746, Republic of Korea. E-mail: dykwon@kfri.re.kr; Sung Kwang Park, Renal Regeneration Laboratory, Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk National University Medical School, 634-18, Keum-Am Dong, Jeonju 561-712, Republic of Korea. E-mail: parksk@chonbuk.ac.kr

³The first two authors contributed equally to this work.

Received 8 October 2007; Revised 7 May 2008; Accepted 11 June 2008; Published online 20 August 2008.

Abstract

Oxidative stress and inflammation contribute to the pathogenesis of cisplatin-induced nephrotoxicity. We found that genistein, a tyrosine kinase inhibitor with broad specificities, and which also has estrogen-like activity, had protective effects on cisplatin-induced renal injury in mice. Genistein significantly decreased reactive oxygen species production, the expression of intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 proteins, as well as the translocation of the p65 subunit of nuclear factor-B into the nucleus and the infiltration of macrophages, all of which were increased in the kidney by cisplatin treatment. Genistein also decreased cisplatin-induced apoptosis by regulating p53 induction in kidney. Genistein significantly reduced reactive oxygen species production in cisplatin-treated normal human kidney HK-2 cells. These studies show that genistein or similar compounds might be useful in prevention of cisplatin-induced renal injury.