Cytoprotective Mechanism of Cyanidin and Delphinidin against Oxidative Stress-Induced Tenofibroblast Deathopen access
- Authors
- Nam, Dae Cheol; Hah, Young Sool; Nam, Jung Been; Kim, Ra Jeong; Park, Hyung Bin
- Issue Date
- 1-Jul-2016
- Publisher
- KOREAN SOC APPLIED PHARMACOLOGY
- Keywords
- Cyanidin; Delphinidin; Apoptosis; Rotator cuff; Tenofibroblast
- Citation
- BIOMOLECULES & THERAPEUTICS, v.24, no.4, pp 426 - 432
- Pages
- 7
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- BIOMOLECULES & THERAPEUTICS
- Volume
- 24
- Number
- 4
- Start Page
- 426
- End Page
- 432
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/15377
- DOI
- 10.4062/biomolther.2015.169
- ISSN
- 1976-9148
2005-4483
- Abstract
- Age-related rotator cuff tendon degeneration is related to tenofibroblast apoptosis. Anthocyanins reduce oxidative stress-induced apoptotic cell death in tenofibroblasts. The current study investigated the presence of cell protective effects in cyanidin and delphinidin, the most common aglycon forms of anthocyanins. We determined whether these anthocyanidins have antiapoptotic and antinecrotic effects in tenofibroblasts exposed to H2O2, and evaluated their biomolecular mechanisms. Both cyanidin and delphinidin inhibited H2O2-induced apoptosis in a dose-dependent manner. However, at concentrations of 100 mu g/ml or greater, delphinidin showed cytotoxicity against tenofibroblasts and a decreased antinecrotic effect. Cyanidin and delphinidin both showed inhibitory effects on the H2O2-induced increase in intracellular ROS formation and the activation of ERK1/2 and JNK. In conclusion, both cyanidin and delphinidin have cytoprotective effects on cultured tenofibroblasts exposed to H2O2. These results suggest that cyanidin and delphinidin are both beneficial for the treatment of oxidative stress-mediated tenofibroblast cell death, but their working concentrations are different.
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