Cargando…

A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice

Accumulating evidence demonstrated that hydrogen sulfide (H(2)S) is highly involved in inflammation, oxidative stress, and apoptosis and contributes to the pathogenesis of kidney diseases. However, the role of H(2)S in cisplatin nephrotoxicity is still debatable. Here we investigated the effect of G...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Mi, Jia, Zhanjun, Sun, Ying, Zhang, Aihua, Yang, Tianxin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4906217/
https://www.ncbi.nlm.nih.gov/pubmed/27340345
http://dx.doi.org/10.1155/2016/8145785
_version_ 1782437385156427776
author Liu, Mi
Jia, Zhanjun
Sun, Ying
Zhang, Aihua
Yang, Tianxin
author_facet Liu, Mi
Jia, Zhanjun
Sun, Ying
Zhang, Aihua
Yang, Tianxin
author_sort Liu, Mi
collection PubMed
description Accumulating evidence demonstrated that hydrogen sulfide (H(2)S) is highly involved in inflammation, oxidative stress, and apoptosis and contributes to the pathogenesis of kidney diseases. However, the role of H(2)S in cisplatin nephrotoxicity is still debatable. Here we investigated the effect of GYY4137, a novel slow-releasing H(2)S donor, on cisplatin nephrotoxicity in mice. Male C57BL/6 mice were pretreated with GYY4137 for 72 h prior to cisplatin injection. After cisplatin treatment for 72 h, mice developed obvious renal dysfunction and kidney injury as evidenced by elevated blood urea nitrogen (BUN) and histological damage. Consistently, these mice also showed increased proinflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and/or kidney tissues. Meanwhile, circulating thiobarbituric aid-reactive substances (TBARS) and renal apoptotic indices including caspase-3, Bak, and Bax were all elevated. However, application of GYY4137 further aggravated renal dysfunction and kidney structural injury in line with promoted inflammation, oxidative stress, and apoptotic response following cisplatin treatment. Taken together, our results suggested that GYY4137 exacerbated cisplatin-induced nephrotoxicity in mice possibly through promoting inflammation, oxidative stress, and apoptotic response.
format Online
Article
Text
id pubmed-4906217
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-49062172016-06-23 A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice Liu, Mi Jia, Zhanjun Sun, Ying Zhang, Aihua Yang, Tianxin Mediators Inflamm Research Article Accumulating evidence demonstrated that hydrogen sulfide (H(2)S) is highly involved in inflammation, oxidative stress, and apoptosis and contributes to the pathogenesis of kidney diseases. However, the role of H(2)S in cisplatin nephrotoxicity is still debatable. Here we investigated the effect of GYY4137, a novel slow-releasing H(2)S donor, on cisplatin nephrotoxicity in mice. Male C57BL/6 mice were pretreated with GYY4137 for 72 h prior to cisplatin injection. After cisplatin treatment for 72 h, mice developed obvious renal dysfunction and kidney injury as evidenced by elevated blood urea nitrogen (BUN) and histological damage. Consistently, these mice also showed increased proinflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and/or kidney tissues. Meanwhile, circulating thiobarbituric aid-reactive substances (TBARS) and renal apoptotic indices including caspase-3, Bak, and Bax were all elevated. However, application of GYY4137 further aggravated renal dysfunction and kidney structural injury in line with promoted inflammation, oxidative stress, and apoptotic response following cisplatin treatment. Taken together, our results suggested that GYY4137 exacerbated cisplatin-induced nephrotoxicity in mice possibly through promoting inflammation, oxidative stress, and apoptotic response. Hindawi Publishing Corporation 2016 2016-05-31 /pmc/articles/PMC4906217/ /pubmed/27340345 http://dx.doi.org/10.1155/2016/8145785 Text en Copyright © 2016 Mi Liu et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liu, Mi
Jia, Zhanjun
Sun, Ying
Zhang, Aihua
Yang, Tianxin
A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title_full A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title_fullStr A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title_full_unstemmed A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title_short A H(2)S Donor GYY4137 Exacerbates Cisplatin-Induced Nephrotoxicity in Mice
title_sort h(2)s donor gyy4137 exacerbates cisplatin-induced nephrotoxicity in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4906217/
https://www.ncbi.nlm.nih.gov/pubmed/27340345
http://dx.doi.org/10.1155/2016/8145785
work_keys_str_mv AT liumi ah2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT jiazhanjun ah2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT sunying ah2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT zhangaihua ah2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT yangtianxin ah2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT liumi h2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT jiazhanjun h2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT sunying h2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT zhangaihua h2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice
AT yangtianxin h2sdonorgyy4137exacerbatescisplatininducednephrotoxicityinmice