The Cytoprotective Effect of Petalonia binghamiae Methanol Extract against Oxidative Stress in C2C12 Myoblasts: Mediation by Upregulation of Heme Oxygenase-1 and Nuclear Factor-Erythroid 2 Related Factor 2

• Published in: Marine drugs Vol. 13; no. 5; pp. 2666 - 2679
• Main Authors: Kang, Ji Sook, Choi, Il-Whan, Han, Min Ho, Lee, Dae-Sung, Kim, Gi-Young, Hwang, Hye Jin, Kim, Byung Woo, Kim, Cheol Min, Yoo, Young Hyun, Choi, Yung Hyun
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 29.04.2015; MDPI
• Subjects: Animals; Antioxidants - metabolism; Apoptosis - drug effects; Cells, Cultured; DNA damage; DNA Damage - drug effects; Heme Oxygenase-1 - metabolism; Hydrogen Peroxide - metabolism; Methanol - chemistry; Mice; Myoblasts - drug effects; Myoblasts - metabolism; NF-E2-Related Factor 2 - metabolism; Nrf2/HO-1; oxidative stress; Oxidative Stress - drug effects; Petalonia; Petalonia binghamiae; Phaeophyceae - chemistry; Phosphorylation - drug effects; Protective Agents - pharmacology; Reactive Oxygen Species - metabolism; ROS; Signal Transduction - drug effects; Up-Regulation - drug effects
• DOI: 10.3390/md13052666
• ISSN: 1660-3397

This study was designed to examine the protective effects of the marine brown algae Petalonia binghamiae against oxidative stress-induced cellular damage and to elucidate the underlying mechanisms. P. binghamiae methanol extract (PBME) prevented hydrogen peroxide (H2O2)-induced growth inhibition and exhibited scavenging activity against intracellular reactive oxygen species (ROS) induced by H2O2 in mouse-derived C2C12 myoblasts. PBME also significantly attenuated H2O2-induced comet tail formation in a comet assay, histone γH2A.X phosphorylation, and annexin V-positive cells, suggesting that PBME prevented H2O2-induced cellular DNA damage and apoptotic cell death. Furthermore, PBME increased the levels of heme oxygenase-1 (HO-1), a potent antioxidant enzyme, associated with the induction of nuclear factor-erythroid 2 related factor 2 (Nrf2). However, zinc protoporphyrin IX, a HO-1 competitive inhibitor, significantly abolished the protective effects of PBME on H2O2-induced ROS generation, growth inhibition, and apoptosis. Collectively, these results demonstrate that PBME augments the antioxidant defense capacity through activation of the Nrf2/HO-1 pathway.