Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

Objective: The present study investigated the possible effect of fenofibrate (peroxisome proliferator-activated receptors-α agonist) in nicotine-induced acute kidney injury (AKI) in rats. Materials and Methods: Nicotine (2 mg/kg/day, intraperitoneally) was administered for 4 weeks to induce AKI in r...

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Autores principales:	Vishal Arvind Chakkarwar, Pravin Kawtikwar
Formato:	article
Lenguaje:	EN
Publicado:	Wolters Kluwer Medknow Publications 2021
Materias:	acute kidney injury fenofibrate nephroprotective nicotine Diseases of the genitourinary system. Urology RC870-923
Acceso en línea:	https://doaj.org/article/537b9d620f7e4598a6c09649aaf08a0d
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spelling	oai:doaj.org-article:537b9d620f7e4598a6c09649aaf08a0d2021-12-02T17:28:22ZFenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase0971-40651998-366210.4103/ijn.IJN_380_20https://doaj.org/article/537b9d620f7e4598a6c09649aaf08a0d2021-01-01T00:00:00Zhttp://www.indianjnephrol.org/article.asp?issn=0971-4065;year=2021;volume=31;issue=5;spage=435;epage=441;aulast=Chakkarwarhttps://doaj.org/toc/0971-4065https://doaj.org/toc/1998-3662Objective: The present study investigated the possible effect of fenofibrate (peroxisome proliferator-activated receptors-α agonist) in nicotine-induced acute kidney injury (AKI) in rats. Materials and Methods: Nicotine (2 mg/kg/day, intraperitoneally) was administered for 4 weeks to induce AKI in rats. Lipid profile and renal oxidative stress were measured and expression of mRNA for eNOS was assessed using reverse transcription-polymerase chain reaction along with serum and renal tissue nitrite levels. Serum creatinine, blood urea nitrogen and microproteinuria were estimated along with the kidney histology, as markers of kidney function. Treatment with fenofibrate (30 mg/kg per oral, 4 weeks) was initiated 3 days before the administration of nicotine and continued for 4 weeks from the day of administration of nicotine. Results: Nicotine administered rats developed apparent AKI confirmed by elevated markers of kidney function and noticeable glomerulosclerosis and tubular cell degeneration. Nicotine decreases the expression of mRNA for eNOS, along with serum and renal tissue nitrite levels. In addition, nicotine showed significantly lipid alteration beside decrease oxidative stress, assessed in terms of increase in serum thiobarbituric acid reactive substance and a marked decrease in tissue reduced glutathione. However, fenofibrate significantly prevented the development of nicotine-AKI by reducing serum creatinine, BUN, and urinary protein, normalizing the lipid profile, reducing renal oxidative stress, increases the eNOS expression and concentration of serum and renal nitrate levels. Conclusion: Fenofibrate attenuates nicotine-induced AKI, via its antihyperlipidemic and antioxidant property. Moreover, fenofibrate induced upregulation of eNOS expression additionally play key roles in the improvement of nicotine-induced AKI could be the future alternative.Vishal Arvind ChakkarwarPravin KawtikwarWolters Kluwer Medknow Publicationsarticleacute kidney injuryfenofibratenephroprotectivenicotineDiseases of the genitourinary system. UrologyRC870-923ENIndian Journal of Nephrology, Vol 31, Iss 5, Pp 435-441 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	acute kidney injury fenofibrate nephroprotective nicotine Diseases of the genitourinary system. Urology RC870-923
spellingShingle	acute kidney injury fenofibrate nephroprotective nicotine Diseases of the genitourinary system. Urology RC870-923 Vishal Arvind Chakkarwar Pravin Kawtikwar Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
description	Objective: The present study investigated the possible effect of fenofibrate (peroxisome proliferator-activated receptors-α agonist) in nicotine-induced acute kidney injury (AKI) in rats. Materials and Methods: Nicotine (2 mg/kg/day, intraperitoneally) was administered for 4 weeks to induce AKI in rats. Lipid profile and renal oxidative stress were measured and expression of mRNA for eNOS was assessed using reverse transcription-polymerase chain reaction along with serum and renal tissue nitrite levels. Serum creatinine, blood urea nitrogen and microproteinuria were estimated along with the kidney histology, as markers of kidney function. Treatment with fenofibrate (30 mg/kg per oral, 4 weeks) was initiated 3 days before the administration of nicotine and continued for 4 weeks from the day of administration of nicotine. Results: Nicotine administered rats developed apparent AKI confirmed by elevated markers of kidney function and noticeable glomerulosclerosis and tubular cell degeneration. Nicotine decreases the expression of mRNA for eNOS, along with serum and renal tissue nitrite levels. In addition, nicotine showed significantly lipid alteration beside decrease oxidative stress, assessed in terms of increase in serum thiobarbituric acid reactive substance and a marked decrease in tissue reduced glutathione. However, fenofibrate significantly prevented the development of nicotine-AKI by reducing serum creatinine, BUN, and urinary protein, normalizing the lipid profile, reducing renal oxidative stress, increases the eNOS expression and concentration of serum and renal nitrate levels. Conclusion: Fenofibrate attenuates nicotine-induced AKI, via its antihyperlipidemic and antioxidant property. Moreover, fenofibrate induced upregulation of eNOS expression additionally play key roles in the improvement of nicotine-induced AKI could be the future alternative.
format	article
author	Vishal Arvind Chakkarwar Pravin Kawtikwar
author_facet	Vishal Arvind Chakkarwar Pravin Kawtikwar
author_sort	Vishal Arvind Chakkarwar
title	Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
title_short	Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
title_full	Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
title_fullStr	Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
title_full_unstemmed	Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase
title_sort	fenofibrate prevents nicotine-induced acute kidney injury: possible involvement of endothelial nitric oxide synthase
publisher	Wolters Kluwer Medknow Publications
publishDate	2021
url	https://doaj.org/article/537b9d620f7e4598a6c09649aaf08a0d
work_keys_str_mv	AT vishalarvindchakkarwar fenofibratepreventsnicotineinducedacutekidneyinjurypossibleinvolvementofendothelialnitricoxidesynthase AT pravinkawtikwar fenofibratepreventsnicotineinducedacutekidneyinjurypossibleinvolvementofendothelialnitricoxidesynthase
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Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase

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