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Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities

INTRODUCTION: long-term environmental and occupational exposure to lead, which is a ubiquitous industrial pollutant, causes significant damage to tissues of kidney. This report aims to address this debilitating issue. A natural polyphenolic compound, Ellagic acid (EA) is having numerous potential me...

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Autores principales: Bhattacharjee, Ananya, Kulkarni, Venkatrao H., Chakraborty, Manodeep, Habbu, Prasanna V., Ray, Animikh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809373/
https://www.ncbi.nlm.nih.gov/pubmed/33490681
http://dx.doi.org/10.1016/j.heliyon.2021.e05921
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author Bhattacharjee, Ananya
Kulkarni, Venkatrao H.
Chakraborty, Manodeep
Habbu, Prasanna V.
Ray, Animikh
author_facet Bhattacharjee, Ananya
Kulkarni, Venkatrao H.
Chakraborty, Manodeep
Habbu, Prasanna V.
Ray, Animikh
author_sort Bhattacharjee, Ananya
collection PubMed
description INTRODUCTION: long-term environmental and occupational exposure to lead, which is a ubiquitous industrial pollutant, causes significant damage to tissues of kidney. This report aims to address this debilitating issue. A natural polyphenolic compound, Ellagic acid (EA) is having numerous potential medicinal properties. In this present study nephroprotective effects of EA has been evaluated in a rodent model with lead-induced toxicity. METHODS: Rats were treated with EA doses of 50 mg/kg and 25 mg/kg and simultaneously co-administered with lead acetate (60 mg/kg) for 2 months through oral route. The extent to which EA treatment provides nephroprotective effect was estimated by measurement of serum biomarkers, tissue antioxidants, inflammatory mediators, apoptosis, autophagy pathway and histological examination. RESULTS: EA treatment caused significant restoration in the level of serum biomarkers, tissue antioxidants and histological architecture of renal tissue. Treatment with either of the doses of EA causes restoration of pro-inflammatory mediators to approximately pre-exposure concentration. This phenomena is caused by suppression of expression levels of inflammatory molecules like tumour necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), interleukin-6 (IL-6), and interleukin-1β (IL-1β), as well as functional expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Moreover, it was also observed that EA suppressed apoptotic and autophagic pathway by reduction of expression of light chain 3B (LC3B) level which are the oxidative DNA damage markers of renal tissue. CONCLUSION: It can be safely concluded that EA provides protection against lead-induced nephrotoxicity to a significant degree.
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spelling pubmed-78093732021-01-22 Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities Bhattacharjee, Ananya Kulkarni, Venkatrao H. Chakraborty, Manodeep Habbu, Prasanna V. Ray, Animikh Heliyon Research Article INTRODUCTION: long-term environmental and occupational exposure to lead, which is a ubiquitous industrial pollutant, causes significant damage to tissues of kidney. This report aims to address this debilitating issue. A natural polyphenolic compound, Ellagic acid (EA) is having numerous potential medicinal properties. In this present study nephroprotective effects of EA has been evaluated in a rodent model with lead-induced toxicity. METHODS: Rats were treated with EA doses of 50 mg/kg and 25 mg/kg and simultaneously co-administered with lead acetate (60 mg/kg) for 2 months through oral route. The extent to which EA treatment provides nephroprotective effect was estimated by measurement of serum biomarkers, tissue antioxidants, inflammatory mediators, apoptosis, autophagy pathway and histological examination. RESULTS: EA treatment caused significant restoration in the level of serum biomarkers, tissue antioxidants and histological architecture of renal tissue. Treatment with either of the doses of EA causes restoration of pro-inflammatory mediators to approximately pre-exposure concentration. This phenomena is caused by suppression of expression levels of inflammatory molecules like tumour necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), interleukin-6 (IL-6), and interleukin-1β (IL-1β), as well as functional expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Moreover, it was also observed that EA suppressed apoptotic and autophagic pathway by reduction of expression of light chain 3B (LC3B) level which are the oxidative DNA damage markers of renal tissue. CONCLUSION: It can be safely concluded that EA provides protection against lead-induced nephrotoxicity to a significant degree. Elsevier 2021-01-08 /pmc/articles/PMC7809373/ /pubmed/33490681 http://dx.doi.org/10.1016/j.heliyon.2021.e05921 Text en © 2021 The Authors http://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 Research Article
Bhattacharjee, Ananya
Kulkarni, Venkatrao H.
Chakraborty, Manodeep
Habbu, Prasanna V.
Ray, Animikh
Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title_full Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title_fullStr Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title_full_unstemmed Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title_short Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
title_sort ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809373/
https://www.ncbi.nlm.nih.gov/pubmed/33490681
http://dx.doi.org/10.1016/j.heliyon.2021.e05921
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