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Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice

Context: Currently, the outcomes of the use of cisplatin in cancer therapy is limited by nephrotoxicity. Objective: This study aims to investigate the nephroprotective role of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice. Materials and methods: Adult female Wistar Albino m...

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Autores principales: Hassan, Samar M., Khalaf , Marwa M., Sadek, Sawsan A., Abo-Youssef, Amira M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6130592/
https://www.ncbi.nlm.nih.gov/pubmed/28064632
http://dx.doi.org/10.1080/13880209.2016.1275704
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author Hassan, Samar M.
Khalaf , Marwa M.
Sadek, Sawsan A.
Abo-Youssef, Amira M.
author_facet Hassan, Samar M.
Khalaf , Marwa M.
Sadek, Sawsan A.
Abo-Youssef, Amira M.
author_sort Hassan, Samar M.
collection PubMed
description Context: Currently, the outcomes of the use of cisplatin in cancer therapy is limited by nephrotoxicity. Objective: This study aims to investigate the nephroprotective role of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice. Materials and methods: Adult female Wistar Albino mice were divided into eight groups (n = 8). Group I served as normal control. Groups II, III and IV received apigenin (3 mg/kg, i.p.), myricetin (3 mg/kg, i.p.) or their combination respectively, for seven days. Group V served as positive control group, received vehicles for seven days and cisplatin (7.5 mg/kg, i.p.) for three days starting at day five. Groups VI, VII and VIII received apigenin, myricetin or their combination, respectively for seven days as well as cisplatin injection for three days starting at day five. by the end of the experimental period, a biochemical study involving, nephrotoxicity markers [serum creatinine (Cr) and blood urea nitrogen (BUN)], apoptotic marker [caspase 3], inflammatory mediators [tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), cyclooxygenase I and II (COXI, COXII)] and oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH) and catalase] was conducted. In addition, renal histopathological alterations were evaluated. Results: Apigenin, myricetin and their combination significantly reduced blood BUN, serum Cr, caspase-3TNF-α, IL-6, COXI and COXII, MDA levels and significantly increased GSH level and catalase activity parallel to, histopathological improvement in kidney tissues. Discussion and conclusion: Apigenin and myricetin exhibited a protective and promising preventive strategy against cisplatin-induced nephrotoxicity due to their antioxidant and anti-inflammatory effects.
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spelling pubmed-61305922018-09-27 Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice Hassan, Samar M. Khalaf , Marwa M. Sadek, Sawsan A. Abo-Youssef, Amira M. Pharm Biol Research Article Context: Currently, the outcomes of the use of cisplatin in cancer therapy is limited by nephrotoxicity. Objective: This study aims to investigate the nephroprotective role of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice. Materials and methods: Adult female Wistar Albino mice were divided into eight groups (n = 8). Group I served as normal control. Groups II, III and IV received apigenin (3 mg/kg, i.p.), myricetin (3 mg/kg, i.p.) or their combination respectively, for seven days. Group V served as positive control group, received vehicles for seven days and cisplatin (7.5 mg/kg, i.p.) for three days starting at day five. Groups VI, VII and VIII received apigenin, myricetin or their combination, respectively for seven days as well as cisplatin injection for three days starting at day five. by the end of the experimental period, a biochemical study involving, nephrotoxicity markers [serum creatinine (Cr) and blood urea nitrogen (BUN)], apoptotic marker [caspase 3], inflammatory mediators [tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), cyclooxygenase I and II (COXI, COXII)] and oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH) and catalase] was conducted. In addition, renal histopathological alterations were evaluated. Results: Apigenin, myricetin and their combination significantly reduced blood BUN, serum Cr, caspase-3TNF-α, IL-6, COXI and COXII, MDA levels and significantly increased GSH level and catalase activity parallel to, histopathological improvement in kidney tissues. Discussion and conclusion: Apigenin and myricetin exhibited a protective and promising preventive strategy against cisplatin-induced nephrotoxicity due to their antioxidant and anti-inflammatory effects. Taylor & Francis 2017-01-09 /pmc/articles/PMC6130592/ /pubmed/28064632 http://dx.doi.org/10.1080/13880209.2016.1275704 Text en © 2017 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Hassan, Samar M.
Khalaf , Marwa M.
Sadek, Sawsan A.
Abo-Youssef, Amira M.
Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title_full Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title_fullStr Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title_full_unstemmed Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title_short Protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
title_sort protective effects of apigenin and myricetin against cisplatin-induced nephrotoxicity in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6130592/
https://www.ncbi.nlm.nih.gov/pubmed/28064632
http://dx.doi.org/10.1080/13880209.2016.1275704
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