• Users Online: 473
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Contacts Login 
ORIGINAL ARTICLE
Year : 2021  |  Volume : 41  |  Issue : 3  |  Page : 146-152

Estrogen deficiency accompanied by oxidative stress sustains heme oxygenase 1 expression in cardiomyocytes of ovariectomized rats


1 Department and Graduate Institute of Pharmacology, National Defense Medical Center, Taipei, Taiwan
2 Department of Surgery, Division of Cardiovascular Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
3 Department of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan
4 Department and Graduate Institute of Pharmacology; Department of Pharmacy Practice, Tri-Service General Hospital, National Defense National Defense Medical Center, Taipei, Taiwan

Correspondence Address:
Dr. Hsin-Hsueh Shen
Department and Graduate Institute of Pharmacology, National Defense Medical Center, No. 161, Section 6, Min-Chuan East Road, Taipei 114
Taiwan
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmedsci.jmedsci_175_20

Rights and Permissions

Background: Estrogen deficiency is one of the main causes of cardiovascular diseases (CVDs) after menopause, accompanied with the upregulation of oxidative stress. Two isoforms of heme oxygenase (HO), HO-1 and HO-2, have been implicated in the cytoprotective effects via the antioxidant and anti-inflammatory capacities. Aims: This study aimed to investigate the time-course of HO-1 and HO-2 expression in the cardiac tissue of ovariectomized rats and whether oxidative stress is involved in the regulation of HO alteration. Methods: Adult female rats were ovariectomized bilaterally to induce estrogen deficiency and randomly divided into (1) Sham, (2) ovariectomy (Ovx), (3) Ovx + E2 (17β estradiol, 50 μg/kg/day, intramuscular), and (4) Ovx + tempol (1 mM in drinking water, a superoxide dismutase [SOD] mimetic). Rats were sacrificed 12 weeks after Ovx; blood and myocardium samples were collected. Results: Showed that plasma E2 levels of Ovx and Ovx + tempol groups were significantly reduced as compared to Sham group after 4 weeks of Ovx. Superoxide anion in the cardiac tissue was significantly elevated 2 weeks after Ovx, and the increase was drastically reversed by the treatment with E2 and tempol. In addition, Ovx rats showed significantly higher levels of oxidized glutathione (GSSG) than those of Sham group, which were also significantly reduced by E2 and tempol administration. Western blot analysis indicated that HO-1 expression was significantly induced 1 week after Ovx and sustained at high levels until 12 weeks. E2 replacement did not immediately reverse HO-1 until treatment for 4 weeks as well as tempol administration for 5 weeks. Expression of the constitutive enzymes HO-2 did not show significant differences between Sham and Ovx groups, and E2 or tempol administration had no effect on cardiac HO-2 protein expression. Conclusion: E2 deficiency induced upregulation of superoxide anion in the myocardium, which might be the major contributor to the sustained HO-1 expression as adaptive responses to oxidative stress. This study provides new insight into the pathogenesis of CVDs after menopause.


[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
    Viewed296    
    Printed28    
    Emailed0    
    PDF Downloaded33    
    Comments [Add]    

Recommend this journal