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Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats
Though several previous studies reported the in vitro and in vivo antioxidant effect of kinetin (Kn), details on its action in cisplatin-induced toxicity are still scarce. In this study we evaluated, for the first time, the effects of kinetin in cisplatin (cp)- induced liver and lymphocyte toxicity...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312964/ https://www.ncbi.nlm.nih.gov/pubmed/35884925 http://dx.doi.org/10.3390/biomedicines10071620 |
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author | Fathy, Moustafa Darwish, Mostafa A. Abdelhamid, Al-Shaimaa M. Alrashedy, Gehad M. Othman, Othman Ali Naseem, Muhammad Dandekar, Thomas Othman, Eman M. |
author_facet | Fathy, Moustafa Darwish, Mostafa A. Abdelhamid, Al-Shaimaa M. Alrashedy, Gehad M. Othman, Othman Ali Naseem, Muhammad Dandekar, Thomas Othman, Eman M. |
author_sort | Fathy, Moustafa |
collection | PubMed |
description | Though several previous studies reported the in vitro and in vivo antioxidant effect of kinetin (Kn), details on its action in cisplatin-induced toxicity are still scarce. In this study we evaluated, for the first time, the effects of kinetin in cisplatin (cp)- induced liver and lymphocyte toxicity in rats. Wistar male albino rats were divided into nine groups: (i) the control (C), (ii) groups 2,3 and 4, which received 0.25, 0.5 and 1 mg/kg kinetin for 10 days; (iii) the cisplatin (cp) group, which received a single intraperitoneal injection of CP (7.0 mg/kg); and (iv) groups 6, 7, 8 and 9, which received, for 10 days, 0.25, 0.5 and 1 mg/kg kinetin or 200 mg/kg vitamin C, respectively, and Cp on the fourth day. CP-injected rats showed a significant impairment in biochemical, oxidative stress and inflammatory parameters in hepatic tissue and lymphocytes. PCR showed a profound increase in caspase-3, and a significant decline in AKT gene expression. Intriguingly, Kn treatment restored the biochemical, redox status and inflammatory parameters. Hepatic AKT and caspase-3 expression as well as CD95 levels in lymphocytes were also restored. In conclusion, Kn mitigated oxidative imbalance, inflammation and apoptosis in CP-induced liver and lymphocyte toxicity; therefore, it can be considered as a promising therapy. |
format | Online Article Text |
id | pubmed-9312964 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-93129642022-07-26 Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats Fathy, Moustafa Darwish, Mostafa A. Abdelhamid, Al-Shaimaa M. Alrashedy, Gehad M. Othman, Othman Ali Naseem, Muhammad Dandekar, Thomas Othman, Eman M. Biomedicines Article Though several previous studies reported the in vitro and in vivo antioxidant effect of kinetin (Kn), details on its action in cisplatin-induced toxicity are still scarce. In this study we evaluated, for the first time, the effects of kinetin in cisplatin (cp)- induced liver and lymphocyte toxicity in rats. Wistar male albino rats were divided into nine groups: (i) the control (C), (ii) groups 2,3 and 4, which received 0.25, 0.5 and 1 mg/kg kinetin for 10 days; (iii) the cisplatin (cp) group, which received a single intraperitoneal injection of CP (7.0 mg/kg); and (iv) groups 6, 7, 8 and 9, which received, for 10 days, 0.25, 0.5 and 1 mg/kg kinetin or 200 mg/kg vitamin C, respectively, and Cp on the fourth day. CP-injected rats showed a significant impairment in biochemical, oxidative stress and inflammatory parameters in hepatic tissue and lymphocytes. PCR showed a profound increase in caspase-3, and a significant decline in AKT gene expression. Intriguingly, Kn treatment restored the biochemical, redox status and inflammatory parameters. Hepatic AKT and caspase-3 expression as well as CD95 levels in lymphocytes were also restored. In conclusion, Kn mitigated oxidative imbalance, inflammation and apoptosis in CP-induced liver and lymphocyte toxicity; therefore, it can be considered as a promising therapy. MDPI 2022-07-06 /pmc/articles/PMC9312964/ /pubmed/35884925 http://dx.doi.org/10.3390/biomedicines10071620 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Fathy, Moustafa Darwish, Mostafa A. Abdelhamid, Al-Shaimaa M. Alrashedy, Gehad M. Othman, Othman Ali Naseem, Muhammad Dandekar, Thomas Othman, Eman M. Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title | Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title_full | Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title_fullStr | Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title_full_unstemmed | Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title_short | Kinetin Ameliorates Cisplatin-Induced Hepatotoxicity and Lymphotoxicity via Attenuating Oxidative Damage, Cell Apoptosis and Inflammation in Rats |
title_sort | kinetin ameliorates cisplatin-induced hepatotoxicity and lymphotoxicity via attenuating oxidative damage, cell apoptosis and inflammation in rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312964/ https://www.ncbi.nlm.nih.gov/pubmed/35884925 http://dx.doi.org/10.3390/biomedicines10071620 |
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