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. Autophagy inhibition enhances apoptosis induced by dioscin in Huh7 cells
 
  • Details
Options

Autophagy inhibition enhances apoptosis induced by dioscin in Huh7 cells

Journal
Evidence-based Complementary and Alternative Medicine
Date Issued
2012-01-01
Author(s)
SHUN-FA YANG  
HUI-LING CHIOU  
DOI
10.1155/2012/134512
URI
https://www.scopus.com/pages/publications/84870230222
https://scholars.csmu.edu.tw/handle/123456789/28112
Abstract
Extensive research results support the application of herbal medicine or natural food as an augment during therapy for various cancers. However, the effect of dioscin on tumor cells autophagy has not been clearly clarified. In this study, the unique effects of dioscin on autophagy of hepatoma cells were investigated. Results found that dioscin induced caspase-3- and -9-dependent cell apoptosis in a dose-dependent manner. Moreover, inhibition of ERK1/2 phosphorylation significantly abolished the dioscin-induced apoptosis. In addition, dioscin triggered cell autophagy in early stages. With autophagy inhibitors to hinder the autophagy process, dioscin-induced cell apoptosis was significantly enhanced. An inhibition of caspase activation did not affect the dioscin-induced LC3-II protein expression. Based on the results, we believed that while apoptosis was blocked, dioscin-induced autophagy process also diminished in Huh7 cells. In conclusion, this study indicates that dioscin causes autophagy in Huh7 cells and suggests that dioscin has a cytoprotective effect.
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