Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats

Aim: The aim of this study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in renal protection offered by sinapic acid in cisplatin-induced nephrotoxicity in male rats. Materials and Methods: Nephrotoxicity was induced by single dose of cisplatin (5 mg...

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Main Authors: Hardevinder Pal Singh, Thakur Gurjeet Singh, Randhir Singh
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2020-01-01
Series:Journal of Pharmacy and Bioallied Sciences
Subjects:
Online Access:http://www.jpbsonline.org/article.asp?issn=0975-7406;year=2020;volume=12;issue=2;spage=146;epage=154;aulast=Singh
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author Hardevinder Pal Singh
Thakur Gurjeet Singh
Randhir Singh
author_facet Hardevinder Pal Singh
Thakur Gurjeet Singh
Randhir Singh
author_sort Hardevinder Pal Singh
collection DOAJ
description Aim: The aim of this study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in renal protection offered by sinapic acid in cisplatin-induced nephrotoxicity in male rats. Materials and Methods: Nephrotoxicity was induced by single dose of cisplatin (5 mg/kg, intraperitoneal [i.p.]) in rats. Cisplatin-induced nephrotoxicity was assessed by measuring serum creatinine, creatinine clearance, urea, uric acid, potassium, magnesium levels, fractional excretion of sodium, and microproteinuria in rats. Superoxide anion generation, thiobarbituric acid reactive substances, myeloperoxidase activity, and reduced glutathione levels were measured to assess oxidative stress in renal tissues. Hematoxylin and eosin stain showed renal histological changes. Results: The significant changes in serum and urinary parameters, elevated oxidative stress, and renal histological changes established the induction of nephrotoxicity. Sinapic acid treatment (20 and 40 mg/kg, orally [p.o.]) provides dose-dependent and significant (P < 0.05) nephroprotection against cisplatin-mediated nephrotoxicity in rats. Nephroprotective effect of sinapic acid was abolished by PPAR-γ inhibitor, bisphenol A diglycidyl ether (30 mg/kg, i.p.) in rats. Conclusion: It is concluded that PPAR-γ agonism serves as one of the mechanisms in sinapic acid-mediated renoprotection.
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spelling doaj.art-1e150a4be6034f22bbf00e2cb999247c2022-12-21T23:09:47ZengWolters Kluwer Medknow PublicationsJournal of Pharmacy and Bioallied Sciences0975-74062020-01-0112214615410.4103/jpbs.JPBS_220_19Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in ratsHardevinder Pal SinghThakur Gurjeet SinghRandhir SinghAim: The aim of this study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in renal protection offered by sinapic acid in cisplatin-induced nephrotoxicity in male rats. Materials and Methods: Nephrotoxicity was induced by single dose of cisplatin (5 mg/kg, intraperitoneal [i.p.]) in rats. Cisplatin-induced nephrotoxicity was assessed by measuring serum creatinine, creatinine clearance, urea, uric acid, potassium, magnesium levels, fractional excretion of sodium, and microproteinuria in rats. Superoxide anion generation, thiobarbituric acid reactive substances, myeloperoxidase activity, and reduced glutathione levels were measured to assess oxidative stress in renal tissues. Hematoxylin and eosin stain showed renal histological changes. Results: The significant changes in serum and urinary parameters, elevated oxidative stress, and renal histological changes established the induction of nephrotoxicity. Sinapic acid treatment (20 and 40 mg/kg, orally [p.o.]) provides dose-dependent and significant (P < 0.05) nephroprotection against cisplatin-mediated nephrotoxicity in rats. Nephroprotective effect of sinapic acid was abolished by PPAR-γ inhibitor, bisphenol A diglycidyl ether (30 mg/kg, i.p.) in rats. Conclusion: It is concluded that PPAR-γ agonism serves as one of the mechanisms in sinapic acid-mediated renoprotection.http://www.jpbsonline.org/article.asp?issn=0975-7406;year=2020;volume=12;issue=2;spage=146;epage=154;aulast=Singhbisphenol a diglycidyl ethercisplatinnephrotoxicityoxidative stressperoxisome proliferator-activated receptor-gammarenoprotectionsinapic acid
spellingShingle Hardevinder Pal Singh
Thakur Gurjeet Singh
Randhir Singh
Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
Journal of Pharmacy and Bioallied Sciences
bisphenol a diglycidyl ether
cisplatin
nephrotoxicity
oxidative stress
peroxisome proliferator-activated receptor-gamma
renoprotection
sinapic acid
title Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
title_full Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
title_fullStr Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
title_full_unstemmed Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
title_short Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats
title_sort sinapic acid attenuates cisplatin induced nephrotoxicity through peroxisome proliferator activated receptor gamma agonism in rats
topic bisphenol a diglycidyl ether
cisplatin
nephrotoxicity
oxidative stress
peroxisome proliferator-activated receptor-gamma
renoprotection
sinapic acid
url http://www.jpbsonline.org/article.asp?issn=0975-7406;year=2020;volume=12;issue=2;spage=146;epage=154;aulast=Singh
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AT thakurgurjeetsingh sinapicacidattenuatescisplatininducednephrotoxicitythroughperoxisomeproliferatoractivatedreceptorgammaagonisminrats
AT randhirsingh sinapicacidattenuatescisplatininducednephrotoxicitythroughperoxisomeproliferatoractivatedreceptorgammaagonisminrats