Genistein protects the kidney from cisplatin-induced injury.
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-kappaB 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.
Sung
Mi Jeong
MJ
Food Function Research Center, Korea Food Research Institute, Seongnam, Gyeongki, Republic of Korea.
Kim
Duk Hoon
DH
Jung
Yu Jin
YJ
Kang
Kyung Pyo
KP
Lee
Ae Sin
AS
Lee
Sik
S
Kim
Won
W
Davaatseren
Munkhtugs
M
Hwang
Jin-Taek
JT
Kim
Hyun-Jin
HJ
Kim
Myung Sunny
MS
Kwon
Dae Young
DY
Park
Sung Kwang
SK
D000818:Animals; D015815:Cell Adhesion Molecules / Q000032:analysis; D002460:Cell Line; D002945:Cisplatin / Q000009:adverse effects*; D019833:Genistein / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007674:Kidney Diseases / Q000139:chemically induced* / Q000517:prevention & control*; D051379:Mice; D017382:Reactive Oxygen Species / Q000032:analysis; D051996:Transcription Factor RelA / Q000378:metabolism
D015815:Cell Adhesion Molecules; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA; D019833:Genistein; D002945:Cisplatin