• Users Online: 209
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Browse Articles Search Archives Submit article Instructions Subscribe Contacts Login 
ORIGINAL ARTICLE
Year : 2017  |  Volume : 8  |  Issue : 1  |  Page : 69

Effect of angiotensin-converting enzyme inhibitor on cardiac fibrosis and oxidative stress status in lipopolysaccharide-induced inflammation model in rats


1 Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2 Department of Physiology, School of Medicine, Esfarayen Faculty of Medical Sciences, Esfarayen, Iran
3 Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
4 Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
5 Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Correspondence Address:
Majid Khazaei
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad
Iran
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpvm.IJPVM_322_16

Rights and Permissions

Background: Renin-angiotensin (Ang)-aldosterone system not only plays a key role in the regulation of circulatory homeostasis, but also it acts as a powerful pro-inflammatory mediator. The aim of this study was to evaluate the effect of captopril (Cap), a known Ang-converting enzyme inhibitor, on inflammation-induced cardiac fibrosis, and heart oxidative stress status in lipopolysaccharide (LPS)-induced inflammation in male rats. Methods: Fifty male rats were randomly divided into five groups control, LPS (1 mg/kg/day), LPS + Cap 10 mg/kg, LPS + Cap 50 mg/kg and LPS + Cap 100 mg/kg. After 2 weeks, blood samples were taken, and hearts were harvested for evaluation of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide metabolite in serum and tissue hemogenate, histopathology (hematoxylin and eosin and Masson's trichrome) and oxidative stress status. Results: Serum IL-6 and TNF-α concentration were higher in LPS group compared to control and Cap reduced them, significantly. Heart TNF-α and IL-6 contents in LPS group were significantly higher than control (P < 0.05). The administration of Cap significantly decreased inflammatory markers level to control (P < 0.05). The higher levels of malondialdehyde and lower antioxidative markers (total thiol, superoxide dismutase, and catalase) in the heart were observed in LPS group and treatment by Cap improved them, dose-dependently. Histopathological study revealed cardiac fibrosis and more collagen content in LPS group which significantly improved by Cap treatment. Conclusions: Treatment by Cap reduced cardiac fibrosis possibly through improving oxidative stress status, and it can be considered to increase cardiac compliance in this condition.


[FULL TEXT] [PDF]*
Print this article     Email this article
 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
    Viewed32    
    Printed0    
    Emailed0    
    PDF Downloaded19    
    Comments [Add]    

Recommend this journal