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Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity

BACKGROUND: The last-line agent for gram-negative bacteria that have developed resistance towards commonly used antibiotics is polymyxin E (PolyE). The renal toxicity attributed to this agent limits its use, proper dosing, and eventually its clinical efficacy. Although the exact mechanism of PolyE-i...

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Autores principales: Vazin, Afsaneh, Heidari, Reza, Khodami, Zahra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7280086/
https://www.ncbi.nlm.nih.gov/pubmed/32581601
http://dx.doi.org/10.2147/JEP.S255861
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author Vazin, Afsaneh
Heidari, Reza
Khodami, Zahra
author_facet Vazin, Afsaneh
Heidari, Reza
Khodami, Zahra
author_sort Vazin, Afsaneh
collection PubMed
description BACKGROUND: The last-line agent for gram-negative bacteria that have developed resistance towards commonly used antibiotics is polymyxin E (PolyE). The renal toxicity attributed to this agent limits its use, proper dosing, and eventually its clinical efficacy. Although the exact mechanism of PolyE-induced nephrotoxicity is not obvious, some investigations suggest the role of oxidative stress and its associated events in this complication. Curcumin (CUR) is a potent antioxidant molecule. The aim of the current investigation was the evaluation of the potential nephroprotective properties of CUR in PolyE-treated mice. MATERIALS AND METHODS: Mice were randomly allocated into five groups (n = 8 per group). PolyE (15 mg/kg/day, i.v, for 7 days) alone or in combination with CUR (10, 100 and 200 mg/kg, i.p) were administered to mice. Renal injury biomarkers, in addition to markers of oxidative stress and kidney histopathological alterations, were evaluated. RESULTS: Plasma creatinine (Cr) and blood urine nitrogen (BUN) significantly raised in PolyE group. Oxidative stress biomarkers consisting of reactive oxygen species (ROS) and lipid peroxidation (LPO) also increased, and concomitantly GSH and antioxidant capacity of renal cells significantly decreased following the use of PolyE. Interstitial nephritis, tissue necrosis, and glomerular atrophy were all induced by the use of PolyE in the mice kidney. CUR (10, 100, and 200 mg/kg, i.p) treatment alleviated PolyE-induced oxidative stress and histopathological alterations in the kidney tissue significantly. CONCLUSION: According to the results of this study, CUR has a protective role against renal toxicity induced by PolyE. Hence, more research is necessary until this compound could be clinically applicable to alleviate PolyE-induced renal injury.
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spelling pubmed-72800862020-06-23 Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity Vazin, Afsaneh Heidari, Reza Khodami, Zahra J Exp Pharmacol Original Research BACKGROUND: The last-line agent for gram-negative bacteria that have developed resistance towards commonly used antibiotics is polymyxin E (PolyE). The renal toxicity attributed to this agent limits its use, proper dosing, and eventually its clinical efficacy. Although the exact mechanism of PolyE-induced nephrotoxicity is not obvious, some investigations suggest the role of oxidative stress and its associated events in this complication. Curcumin (CUR) is a potent antioxidant molecule. The aim of the current investigation was the evaluation of the potential nephroprotective properties of CUR in PolyE-treated mice. MATERIALS AND METHODS: Mice were randomly allocated into five groups (n = 8 per group). PolyE (15 mg/kg/day, i.v, for 7 days) alone or in combination with CUR (10, 100 and 200 mg/kg, i.p) were administered to mice. Renal injury biomarkers, in addition to markers of oxidative stress and kidney histopathological alterations, were evaluated. RESULTS: Plasma creatinine (Cr) and blood urine nitrogen (BUN) significantly raised in PolyE group. Oxidative stress biomarkers consisting of reactive oxygen species (ROS) and lipid peroxidation (LPO) also increased, and concomitantly GSH and antioxidant capacity of renal cells significantly decreased following the use of PolyE. Interstitial nephritis, tissue necrosis, and glomerular atrophy were all induced by the use of PolyE in the mice kidney. CUR (10, 100, and 200 mg/kg, i.p) treatment alleviated PolyE-induced oxidative stress and histopathological alterations in the kidney tissue significantly. CONCLUSION: According to the results of this study, CUR has a protective role against renal toxicity induced by PolyE. Hence, more research is necessary until this compound could be clinically applicable to alleviate PolyE-induced renal injury. Dove 2020-06-04 /pmc/articles/PMC7280086/ /pubmed/32581601 http://dx.doi.org/10.2147/JEP.S255861 Text en © 2020 Vazin et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Vazin, Afsaneh
Heidari, Reza
Khodami, Zahra
Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title_full Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title_fullStr Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title_full_unstemmed Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title_short Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity
title_sort curcumin supplementation alleviates polymyxin e-induced nephrotoxicity
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7280086/
https://www.ncbi.nlm.nih.gov/pubmed/32581601
http://dx.doi.org/10.2147/JEP.S255861
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