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Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats

INTRODUCTION: This study investigated the role of diallyl disulfide (DADS) against glycerol-induced nephrotoxicity in rats. Moreover, the role of peroxisome proliferator activated receptor-γ (PPAR-γ) in DADS-mediated renoprotection has been explored. MATERIALS AND METHODS: Male Wistar albino rats we...

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Autores principales: Sharma, Ashwani Kumar, Kaur, Anmoldeep, Kaur, Japneet, Kaur, Gurpreet, Chawla, Apporva, Khanna, Mannan, Kaur, Harmanpreet, Kaur, Harnoor, Kaur, Tajpreet, Singh, Amrit Pal
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8142911/
https://www.ncbi.nlm.nih.gov/pubmed/34084059
http://dx.doi.org/10.4103/jpbs.JPBS_177_20
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author Sharma, Ashwani Kumar
Kaur, Anmoldeep
Kaur, Japneet
Kaur, Gurpreet
Chawla, Apporva
Khanna, Mannan
Kaur, Harmanpreet
Kaur, Harnoor
Kaur, Tajpreet
Singh, Amrit Pal
author_facet Sharma, Ashwani Kumar
Kaur, Anmoldeep
Kaur, Japneet
Kaur, Gurpreet
Chawla, Apporva
Khanna, Mannan
Kaur, Harmanpreet
Kaur, Harnoor
Kaur, Tajpreet
Singh, Amrit Pal
author_sort Sharma, Ashwani Kumar
collection PubMed
description INTRODUCTION: This study investigated the role of diallyl disulfide (DADS) against glycerol-induced nephrotoxicity in rats. Moreover, the role of peroxisome proliferator activated receptor-γ (PPAR-γ) in DADS-mediated renoprotection has been explored. MATERIALS AND METHODS: Male Wistar albino rats were challenged with glycerol (50% w/v, 8 mL/kg intramuscular) to induce nephrotoxicity. Kidney injury was quantified by measuring serum creatinine, creatinine clearance, urea, potassium, fractional excretion of sodium, and microproteinuria in rats. Renal oxidative stress was measured in terms of thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione levels. Hematoxylin–eosin (H&E) and periodic acid Schiff staining of renal samples was done to show histological changes. Glycerol-induced muscle damage was quantified by assaying creatine kinase (CK) levels in rat serum. RESULTS: Administration of glycerol resulted in muscle damage as reflected by significant rise in CK levels in rats. Glycerol intoxication led kidney damage was reflected by significant change in renal biochemical parameters, renal oxidative stress and histological changes in rat kidneys. Administration of DADS attenuated glycerol-induced renal damage. Notably, pretreatment with bisphenol A diglycidyl ether, a PPAR-γ antagonist, abolished DADS renoprotection in rats. CONCLUSION: We conclude that DADS affords protection against glycerol-induced renal damage in rats. Moreover, PPAR-γ plays a key role in DADS-mediated renoprotective effect.
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spelling pubmed-81429112021-06-02 Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats Sharma, Ashwani Kumar Kaur, Anmoldeep Kaur, Japneet Kaur, Gurpreet Chawla, Apporva Khanna, Mannan Kaur, Harmanpreet Kaur, Harnoor Kaur, Tajpreet Singh, Amrit Pal J Pharm Bioallied Sci Original Article INTRODUCTION: This study investigated the role of diallyl disulfide (DADS) against glycerol-induced nephrotoxicity in rats. Moreover, the role of peroxisome proliferator activated receptor-γ (PPAR-γ) in DADS-mediated renoprotection has been explored. MATERIALS AND METHODS: Male Wistar albino rats were challenged with glycerol (50% w/v, 8 mL/kg intramuscular) to induce nephrotoxicity. Kidney injury was quantified by measuring serum creatinine, creatinine clearance, urea, potassium, fractional excretion of sodium, and microproteinuria in rats. Renal oxidative stress was measured in terms of thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione levels. Hematoxylin–eosin (H&E) and periodic acid Schiff staining of renal samples was done to show histological changes. Glycerol-induced muscle damage was quantified by assaying creatine kinase (CK) levels in rat serum. RESULTS: Administration of glycerol resulted in muscle damage as reflected by significant rise in CK levels in rats. Glycerol intoxication led kidney damage was reflected by significant change in renal biochemical parameters, renal oxidative stress and histological changes in rat kidneys. Administration of DADS attenuated glycerol-induced renal damage. Notably, pretreatment with bisphenol A diglycidyl ether, a PPAR-γ antagonist, abolished DADS renoprotection in rats. CONCLUSION: We conclude that DADS affords protection against glycerol-induced renal damage in rats. Moreover, PPAR-γ plays a key role in DADS-mediated renoprotective effect. Wolters Kluwer - Medknow 2021 2020-12-21 /pmc/articles/PMC8142911/ /pubmed/34084059 http://dx.doi.org/10.4103/jpbs.JPBS_177_20 Text en Copyright: © 2020 Journal of Pharmacy and Bioallied Sciences https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Original Article
Sharma, Ashwani Kumar
Kaur, Anmoldeep
Kaur, Japneet
Kaur, Gurpreet
Chawla, Apporva
Khanna, Mannan
Kaur, Harmanpreet
Kaur, Harnoor
Kaur, Tajpreet
Singh, Amrit Pal
Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title_full Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title_fullStr Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title_full_unstemmed Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title_short Ameliorative Role of Diallyl Disulfide Against Glycerol-induced Nephrotoxicity in Rats
title_sort ameliorative role of diallyl disulfide against glycerol-induced nephrotoxicity in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8142911/
https://www.ncbi.nlm.nih.gov/pubmed/34084059
http://dx.doi.org/10.4103/jpbs.JPBS_177_20
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