Repository logo
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
Repository logo
    Communities & Collections
    Research Outputs
    Fundings & Projects
    People
    Organizations
    Statistics
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Chung Shan Medical University
  3. Pure學術人才庫轉入
  4. Sesamin suppresses angiotensin-II-enhanced oxidative stress and hypertrophic markers in H9c2 cells
 
  • Details
Options

Sesamin suppresses angiotensin-II-enhanced oxidative stress and hypertrophic markers in H9c2 cells

Journal
Environmental Toxicology
Date Issued
2023-09-01
Author(s)
PEI-MING CHU  
DOI
10.1002/tox.23853
URI
https://www.scopus.com/pages/publications/85162950984
https://scholars.csmu.edu.tw/handle/123456789/22972
Abstract
Myocardial hypertrophy plays a crucial role in cardiovascular disease (CVD) development. Myocardial hypertrophy is an adaptive response by myocardial cells to stress after cardiac injury to maintain cardiac output and function. Angiotensin II (Ang-II) regulates CVD through the renin-angiotensin-aldosterone system, and its signaling in cardiac myocytes leads to excessive reactive oxygen species (ROS) production, oxidative stress, and inflammation. Sesamin (SA), a natural compound in sesame seeds, has anti-inflammatory and anti-apoptotic effects. This study investigated whether SA could attenuate hypertrophic damage and oxidative injuries in H9c2 cells under Ang-II stimulation. We found that SA decreased the cell surface area. Furthermore, Ang-II treatment reduced Ang-II-increased ANP, BNP, and β-MHC expression. Ang-II enhanced NADPH oxidase activity, ROS formation, and decreased Superoxide Dismutase (SOD) activity. SA treatment reduces Ang-II-caused oxidative injuries. We also found that SA mitigates Ang-II-induced apoptosis and pro-inflammatory responses. In conclusion, SA could attenuate Ang-II-induced cardiac hypertrophic injuries by inhibiting oxidative stress, apoptosis, and inflammation in H9c2 cells. Therefore, SA might be a potential supplement for CVD management.
Type
journal article
Make it your own

DSpace-CRIS can be extensively configured to meet your needs. Decide which information need to be collected and available with fine-grained security. Start updating the theme to match your Institution's web identity.

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science

  • Cookie settings
  • Privacy policy
  • End User Agreement
  • Send Feedback