Open AccessEffect of JNK inhibition on cisplatin-induced renal damage
Author(s) -
Heloísa D. Colletta Francescato,
R. S. Costa,
Fernando Barbosa Júnior,
Terezila Machado Coimbra
Publication year - 2007
Publication title -
nephrology, dialysis, transplantation/nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfm144
Subject(s) - cisplatin , nephrotoxicity , apoptosis , medicine , proinflammatory cytokine , creatinine , western blot , kidney , pharmacology , necrosis , endocrinology , chemistry , biochemistry , inflammation , chemotherapy , gene
Cisplatin therapy is effective against many tumours, however, the nephrotoxicity of this drug is a dose-limiting factor. Apoptosis and necrosis of tubular cells and inflammatory events contribute to the cisplatin-induced nephrotoxicity. Cisplatin promotes increased production of reactive oxygen species, which can activate c-jun N-terminal kinase (JNK) that is a mediator of apoptosis and can lead to increased expression of proinflammatory mediators that could intensify the cytotoxic effects of cisplatin. In this study, we evaluated the effect that SP600125, a selective inhibitor of phosphorylated JNK (p-JNK), has on the renal damage caused by cisplatin use.