Interleukin-6 deficiency accelerates cisplatin-induced acute renal failure but not systemic injury.

摘要: Cisplatin (CDDP), a major chemotherapeutic agent used to treat solid tumors, is known induce acute renal failure (ARF). The progression of tissue injury involves the coordination inflammatory and repair responses. Interleukin-6 (IL-6) has been suggested modulate processes in various injuries. In this study, we analyzed IL-6 regulation during CDDP-induced ARF wild-type (WT) mice determined pathological role using knockout ((-/-)) mice. A correlation between increase serum level blood urea nitrogen was found WT Renal expression most proximal tubular cells suppressor cytokine signaling 3 (SOCS3) gene significantly increased after administration CDDP, suggesting active development. Interestingly, dysfunction occurred soon CDDP became more severe IL-6(-/-) than that contrast, survival rate (50% at 8 days) better (10%). Induction levels proapoptotic Bcl-2 associated X protein (Bax) higher 24h injection. Levels antiapoptotic proteins, Bcl-extra large (Bcl-x(L)), groups were those CDDP-treated throughout experimental period. Bax might contribute development 24h; however, high Bcl-x(L) overcome proapoptosis 72 h These results indicated local systemic elevation contributes produced prevents early stage. deficiency accelerates but not injury.