Indian Journal of Nephrology About us |  Subscription |  e-Alerts  | Feedback | Login   
  Print this page Email this page   Small font sizeDefault font sizeIncrease font size
 Home | Current Issue | Archives| Ahead of print | Search |Instructions |  Editorial Board  

Users Online:138

Official publication of the Indian Society of Nephrology
Ahead of Print

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

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:
Vishal Arvind Chakkarwar,
Department of Pharmacology, SN Institute of Pharmacy, Pusad - 445 204, Maharashtra
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijn.IJN_380_20

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.

Print this article
  Search Pubmed for
    -  Chakkarwar VA
    -  Kawtikwar P
 Citation Manager
 Article Access Statistics
 Reader Comments
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded4    

Recommend this journal

Indian Journal of Nephrology
Published by Wolters Kluwer - Medknow
Online since 20th Sept '07