Main content area

Nephroprotective effects of Lachnum melanin against acute kidney injury induced by cisplatin in mice

Yang, Liuqing, Yang, Qinghua, Li, Jinglei, Hou, Gouhua, Chen, Tingting, Ye, Ming
Process biochemistry 2019 v.83 pp. 198-205
Lachnum, Western blotting, acute kidney injury, apoptosis, blood serum, caspase-3, catalase, cisplatin, creatinine, cytotoxicity, gene expression, glutathione, glutathione peroxidase, inducible nitric oxide synthase, interleukin-1beta, kidneys, malondialdehyde, melanin, mice, mitogen-activated protein kinase, necrosis, neoplasms, nephroprotective effect, oxidative stress, platinum, prostaglandin synthase, protein synthesis, quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction, superoxide dismutase, transcription factor NF-kappa B, tumor necrosis factor-alpha, urea nitrogen, weight loss
The purpose of the present research was to discuss renoprotective effects of intracellular melanin from Lachnum YM156 (LIM) on cisplatin-induced acute kidney injury (AKI) in mice and to explore its possible mechanisms. No cytotoxicity of LIM on the HSF and LO2 cells was found by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cisplatin treatment resulted in noticeable weight loss, raised kidney index, elevated levels of serum creatinine (Cr) and blood urea nitrogen (BUN), and increased platinum accumulation in kidneys. Additionally, renal oxidative stress was evidenced by the increase of malondialdehyde (MDA) concentration and reduction of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) levels after cisplatin administration. The result of quantitative real-time polymerase chain reaction (qRT-PCR) showed that cisplatin treatment significantly elevated the mRNA expression levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in kidneys. Furthermore, western blotting analysis demonstrated that cisplatin administration significantly increased the protein expression levels of nuclear factor-kappaB (NF-κB) p65, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), p-p38 MAPK, p53, caspase 3, cleaved caspase 3 and p38 MAPK, suggesting the inflammation and apoptosis response. However, all these changes were dose-dependently reversed by LIM. Overall, LIM may possess protective effects in cisplatin-induced AKI through suppression of oxidative stress, inflammation and apoptosis.