Publication:
Protective effect of panduratin a on cisplatin-induced apoptosis of human renal proximal tubular cells and acute kidney injury in mice

dc.contributor.authorPenjai Thongnuanjanen_US
dc.contributor.authorSirima Soodvilaien_US
dc.contributor.authorSomsak Fongsupaen_US
dc.contributor.authorNapason Chabangen_US
dc.contributor.authorPornpun Vivithanapornen_US
dc.contributor.authorPatoomratana Tuchindaen_US
dc.contributor.authorSunhapas Soodvilaien_US
dc.contributor.otherRangsit Universityen_US
dc.contributor.otherFaculty of Medicine Ramathibodi Hospital, Mahidol Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherThammasat Universityen_US
dc.date.accessioned2022-08-04T11:21:50Z
dc.date.available2022-08-04T11:21:50Z
dc.date.issued2021-06-01en_US
dc.description.abstractBackground: Cisplatin is an effective chemotherapy but its main side effect, acute kidney injury, limits its use. Panduratin A, a bioactive compound extracted from Boesenbergia rotunda, shows several biological activities such as anti-oxidative effects. The present study investigated the nephroprotective effect of panduratin A on cisplatin-induced renal injury. Methods: We investigated the effect of panduratin A on the toxicity of cisplatin in both mice and human renal cell cultures using RPTEC/TERT1 cells. Results: The results demonstrated that panduratin A ameliorates cisplatin-induced renal toxicity in both mice and RPTEC/ TERT1 cells by reducing apoptosis. Mice treated with a single intraperitoneal (i.p.) injection of cisplatin (20mg/kg body weight (BW)) exhibited renal tubule injury and impaired kidney function as shown by histological examination and increased serum creatinine. Co-administration of panduratin A (50mg/kg BW) orally improved kidney function and ameliorated renal tubule injury of cisplatin by inhibiting activation of extracellular signal-regulated kinase (ERK)1/2 and caspase 3. In human renal proximal tubular cells, cisplatin induced cell apoptosis by activating pro-apoptotic proteins (ERK1/2 and caspase 3), and reducing the anti-apoptotic protein (Bcl-2). These effects were significantly ameliorated by co-treatment with panduratin A. Interestingly, panduratin A did not alter intracellular accumulation of cisplatin. It did not alter the anticancer efficacy of cisplatin in either human colon or non-small cell lung cancer cell lines. Conclusions: The present study highlights panduratin A has a potential protective effect on cisplatin’s nephrotoxicity.en_US
dc.identifier.citationBiological and Pharmaceutical Bulletin. Vol.44, No.6 (2021), 830-837en_US
dc.identifier.doi10.1248/bpb.b21-00036en_US
dc.identifier.issn13475215en_US
dc.identifier.issn09186158en_US
dc.identifier.other2-s2.0-85107194643en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/123456789/78959
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85107194643&origin=inwarden_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleProtective effect of panduratin a on cisplatin-induced apoptosis of human renal proximal tubular cells and acute kidney injury in miceen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85107194643&origin=inwarden_US

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