Cordyceps militaris extract protects human dermal fibroblasts against oxidative stress-induced apoptosis and premature senescence

• Published in: Nutrients Vol. 6; no. 9; pp. 3711 - 3726
• Main Authors: Park, Jun Myoung, Lee, Jong Seok, Lee, Ki Rim, Ha, Suk-Jin, Hong, Eock Kee
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 16-09-2014; MDPI
• Subjects: Aging; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; Biological Products - pharmacology; Biphenyl Compounds - metabolism; Cell death; Cells, Cultured; Cellular Senescence - drug effects; Cordyceps; Cordyceps militaris; Dose-Response Relationship, Drug; fibroblast; Fibroblasts; Fibroblasts - drug effects; Fungi; Humans; Hydrogen Peroxide; Morphology; Oxidative stress; Oxidative Stress - drug effects; Penicillin; Picrates - metabolism; Reactive Oxygen Species - metabolism; Senescence; Skin; United States > US
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu6093711

Oxidative stress induced by reactive oxygen species (ROS) is the major cause of degenerative disorders including aging and disease. In this study, we investigated whether Cordyceps militaris extract (CME) has in vitro protective effects on hydrogen peroxide-induced oxidative stress in human dermal fibroblasts (HDFs). Our results showed that the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity of CME was increased in a dose-dependent manner. We found that hydrogen peroxide treatment in HDFs increased ROS generation and cell death as compared with the control. However, CME improved the survival of HDFs against hydrogen peroxide-induced oxidative stress via inhibition of intracellular ROS production. CME treatment inhibited hydrogen peroxide-induced apoptotic cell death and apoptotic nuclear condensation in HDFs. In addition, CME prevented hydrogen peroxide-induced SA-β-gal-positive cells suggesting CME could inhibit oxidative stress-induced premature senescence. Therefore, these results suggest that CME might have protective effects against oxidative stress-induced premature senescence via scavenging ROS.