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Year : 2021  |  Volume : 31  |  Issue : 5  |  Page : 435--441

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

Vishal Arvind Chakkarwar1, Pravin Kawtikwar2 
1 Department of Pharmacology, SN Institute of Pharmacy, Pusad, Yavatmal; Senior Editor, Prime Editors, SN 40, Besides Prozone Mall, Golden City Centre, Aurangabad, Maharashtra, India
2 Department of Pharmacology, SN Institute of Pharmacy, Pusad, Yavatmal, India

Correspondence Address:
Dr. Vishal Arvind Chakkarwar
Department of Pharmacology, SN Institute of Pharmacy, Pusad - 445 204, Maharashtra
India

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.

How to cite this article:
Chakkarwar VA, Kawtikwar P. Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase.Indian J Nephrol 2021;31:435-441

How to cite this URL:
Chakkarwar VA, Kawtikwar P. Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase. Indian J Nephrol [serial online] 2021 [cited 2021 Dec 1 ];31:435-441
Available from: https://www.indianjnephrol.org/article.asp?issn=0971-4065;year=2021;volume=31;issue=5;spage=435;epage=441;aulast=Chakkarwar;type=0