engleski

NFKB Inhibition Protects against Cisplatin-Induced Acute Kidney Injury

Background: NFKB is a cell signaling pathway important in inflammation and cell survival. Inflammation, acute tubular necrosis (ATN) and apoptosis in the kidney are features of cisplatin-induced AKI. The role of NFKB in cisplatin-induced AKI was determined. Methods: C57BL/6 miceinjected were with cisplatin (Cis) (25 mg/kg) get AKI on day 3. The NFKB (p65) inhibitor JSH-23 (20 mg/kg)IP was injected on day 1 and 2 after cisplatin. Results: Kidney function (BUN, SCr), tubular injury (ATN, serum NGAL), pro- inflammatory cytokines (IL-6, CXCL1, TNF alpha) and MPO activity (a marker of neutrophils and macrophages) were significantlyincreased in AKI and decreased by JSH. On immunoblotof kidney tissuesNFKB (p65), MEKK-1, ERK, JNK, cleaved caspase-3 were significantly increased in AKI and significantly decreased by JSH-23 (n=4 immunoblots/group. Statistical analysis of densitometry data was performed. Conclusions: NFKB inhibition protects against Cis-induced AKI, decreases ATN but not apoptosis, decreases MAPK pathway proteins and pro- inflammatory cytokines and MPO.

NFKB; Cisplatin-Induced Acute Kidney Injury

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