Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/20341
Title: Protective Effects of Cilastatin against Vancomycin-Induced Nephrotoxicity.
Authors: 
Mesh: 
Issue Date: 2015
Citation: Biomed Res Int.2015;(2015):704382
Abstract: Vancomycin is a very effective antibiotic for treatment of severe infections. However, its use in clinical practice is limited by nephrotoxicity. Cilastatin is a dehydropeptidase I inhibitor that acts on the brush border membrane of the proximal tubule to prevent accumulation of imipenem and toxicity. The aim of this study was to investigate the potential protective effect of cilastatin on vancomycin-induced apoptosis and toxicity in cultured renal proximal tubular epithelial cells (RPTECs). Porcine RPTECs were cultured in the presence of vancomycin with and without cilastatin. Vancomycin induced dose-dependent apoptosis in cultured RPTECs, with DNA fragmentation, cell detachment, and a significant decrease in mitochondrial activity. Cilastatin prevented apoptotic events and diminished the antiproliferative effect and severe morphological changes induced by vancomycin. Cilastatin also improved the long-term recovery and survival of RPTECs exposed to vancomycin and partially attenuated vancomycin uptake by RPTECs. On the other hand, cilastatin had no effects on vancomycin-induced necrosis or the bactericidal effect of the antibiotic. This study indicates that cilastatin protects against vancomycin-induced proximal tubule apoptosis and increases cell viability, without compromising the antimicrobial effect of vancomycin. The beneficial effect could be attributed, at least in part, to decreased accumulation of vancomycin in RPTECs.
PMID: 26504822
URI: https://hdl.handle.net/20.500.12530/20341
Rights: openAccess
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. General U. Gregorio Marañón > Artículos

Files in This Item:
File Description SizeFormat 
PMC4609390.pdf3.69 MBAdobe PDFThumbnail
View/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.