| Literature DB >> 33437029 |
Masashi Arita1, Satoshi Watanabe2, Nobumasa Aoki1, Shoji Kuwahara3, Ryo Suzuki1, Sawako Goto4, Yuko Abe1, Miho Takahashi1, Miyuki Sato1, Satoshi Hokari1, Aya Ohtsubo1, Satoshi Shoji1, Koichiro Nozaki1, Kosuke Ichikawa1, Rie Kondo1, Masachika Hayashi1, Yasuyoshi Ohshima1, Hideyuki Kabasawa5, Michihiro Hosojima5, Toshiyuki Koya1, Akihiko Saito4, Toshiaki Kikuchi1.
Abstract
Cisplatin, one of the most active anticancer agents, is widely used in standard chemotherapy for various cancers. Cisplatin is more poorly tolerated than other chemotherapeutic drugs, and the main dose-limiting toxicity of cisplatin is its nephrotoxicity, which is dose-dependent. Although less toxic methods of cisplatin administration have been established, cisplatin-induced nephrotoxicity remains an unsolved problem. Megalin is an endocytic receptor expressed at the apical membrane of proximal tubules. We previously demonstrated that nephrotoxic drugs, including cisplatin, are reabsorbed through megalin and cause proximal tubular cell injury. We further found that cilastatin blocked the binding of cisplatin to megalin in vitro. In this study, we investigated whether cilastatin could reduce cisplatin-induced nephrotoxicity without influencing the antitumor effects of cisplatin. Nephrotoxicity was decreased or absent in mice treated with cisplatin and cilastatin, as determined by kidney injury molecule-1 staining and the blood urea nitrogen content. Combined with cilastatin, a twofold dose of cisplatin was used to successfully treat the mice, which enhanced the antitumor effects of cisplatin but reduced its nephrotoxicity. These findings suggest that we can increase the dose of cisplatin when combined with cilastatin and improve the outcome of cancer patients.Entities:
Year: 2021 PMID: 33437029 PMCID: PMC7804437 DOI: 10.1038/s41598-020-80853-6
Source DB: PubMed Journal: Sci Rep ISSN: 2045-2322 Impact factor: 4.379