Ellagic acid restored lead-induced nephrotoxicity by anti-inflammatory, anti-apoptotic and free radical scavenging activities.
Heliyon
; 7(1): e05921, 2021 Jan.
Article
em En
| MEDLINE
| ID: mdl-33490681
ABSTRACT
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-1ß (IL-1ß), 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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Base de dados:
MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article