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Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats
OBJECTIVE: Gentamicin (GM) is a commonly used aminoglycoside antibiotic, however, renal toxicity has limited its usage. The present study was designed to evaluate the ameliorative effect of Cistanche deserticola on GM-induced nephrotoxicity in rats. METHODS: The nephrotoxicity in rats was induced by...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975639/ https://www.ncbi.nlm.nih.gov/pubmed/36875447 http://dx.doi.org/10.1016/j.chmed.2022.03.008 |
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author | Bai, Ruibin Fan, Jingmin Wang, Yanping Wang, Yan Li, Xue Hu, Fangdi |
author_facet | Bai, Ruibin Fan, Jingmin Wang, Yanping Wang, Yan Li, Xue Hu, Fangdi |
author_sort | Bai, Ruibin |
collection | PubMed |
description | OBJECTIVE: Gentamicin (GM) is a commonly used aminoglycoside antibiotic, however, renal toxicity has limited its usage. The present study was designed to evaluate the ameliorative effect of Cistanche deserticola on GM-induced nephrotoxicity in rats. METHODS: The nephrotoxicity in rats was induced by intraperitoneal administration of GM (100 mg/kg) for 10 consecutive days. Glomerular filtration rate, blood urea nitrogen, creatinine and kidney histopathology were detected to assess the GM-induced nephrotoxicity. The oxidative stress (catalase, superoxide dismutase, glutathione and malondialdehyde) was assessed. The inflammatory response (tumor necrosis factor-α, interleukin-6, myeloperoxidase and nuclear factor-kappa B) and apoptotic marker (Bax and Bcl-2) were also evaluated. RESULTS: The results showed that water and 75% ethanol extracts of C. deserticola (named CDW and CDE, respectively) (100, 200 and 400 mg/kg) in combination with GM could recover the reduction of glomerular filtration rate and enhance the renal endogenous antioxidant capability induced by GM. The increase in the expression of renal inflammatory cytokines (tumor necrosis factor-α and interleukin-6), nuclear protein of nuclear factor-kappa B (p65) and the activity of myeloperoxidase induced by GM was significantly decreased upon CDW or CDE treatment. In addition, CDW or CDE treatment could decrease the Bax protein expression and increase the Bcl-2 protein expression in GM-induced nephrotoxicity in rats significantly. CONCLUSION: The study demonstrated that C. deserticola treatment could attenuate kidney dysfunction and structural damage in rats induced by GM through the reduction of inflammation, oxidative stress and apoptosis. |
format | Online Article Text |
id | pubmed-9975639 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-99756392023-03-02 Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats Bai, Ruibin Fan, Jingmin Wang, Yanping Wang, Yan Li, Xue Hu, Fangdi Chin Herb Med Original Article OBJECTIVE: Gentamicin (GM) is a commonly used aminoglycoside antibiotic, however, renal toxicity has limited its usage. The present study was designed to evaluate the ameliorative effect of Cistanche deserticola on GM-induced nephrotoxicity in rats. METHODS: The nephrotoxicity in rats was induced by intraperitoneal administration of GM (100 mg/kg) for 10 consecutive days. Glomerular filtration rate, blood urea nitrogen, creatinine and kidney histopathology were detected to assess the GM-induced nephrotoxicity. The oxidative stress (catalase, superoxide dismutase, glutathione and malondialdehyde) was assessed. The inflammatory response (tumor necrosis factor-α, interleukin-6, myeloperoxidase and nuclear factor-kappa B) and apoptotic marker (Bax and Bcl-2) were also evaluated. RESULTS: The results showed that water and 75% ethanol extracts of C. deserticola (named CDW and CDE, respectively) (100, 200 and 400 mg/kg) in combination with GM could recover the reduction of glomerular filtration rate and enhance the renal endogenous antioxidant capability induced by GM. The increase in the expression of renal inflammatory cytokines (tumor necrosis factor-α and interleukin-6), nuclear protein of nuclear factor-kappa B (p65) and the activity of myeloperoxidase induced by GM was significantly decreased upon CDW or CDE treatment. In addition, CDW or CDE treatment could decrease the Bax protein expression and increase the Bcl-2 protein expression in GM-induced nephrotoxicity in rats significantly. CONCLUSION: The study demonstrated that C. deserticola treatment could attenuate kidney dysfunction and structural damage in rats induced by GM through the reduction of inflammation, oxidative stress and apoptosis. Elsevier 2022-12-16 /pmc/articles/PMC9975639/ /pubmed/36875447 http://dx.doi.org/10.1016/j.chmed.2022.03.008 Text en © 2022 Editorial Board of Chinese Herbal Medicines Published by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Bai, Ruibin Fan, Jingmin Wang, Yanping Wang, Yan Li, Xue Hu, Fangdi Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title | Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title_full | Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title_fullStr | Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title_full_unstemmed | Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title_short | Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
title_sort | protective effect of cistanche deserticola on gentamicin-induced nephrotoxicity in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975639/ https://www.ncbi.nlm.nih.gov/pubmed/36875447 http://dx.doi.org/10.1016/j.chmed.2022.03.008 |
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