Advertisment

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:271

Official publication of the Indian Society of Nephrology
 ~   Next article
 ~   Previous article
 ~   Table of Contents

 ~   Similar in PUBMED
 ~  Search Pubmed for
 ~  Search in Google Scholar for
 ~Related articles
 ~   Citation Manager
 ~   Access Statistics
 ~   Reader Comments
 ~   Email Alert *
 ~   Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed1021    
    Printed16    
    Emailed0    
    PDF Downloaded14    
    Comments [Add]    

Recommend this journal

 

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

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

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijn.IJN_380_20

Rights and Permissions

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.






[FULL TEXT] [PDF]*


        
Print this article     Email this article

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