Trans -cinnamaldehyde protects C2C12 myoblasts from DNA damage, mitochondrial dysfunction and apoptosis caused by oxidat
- PDF / 1,563,258 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 29 Downloads / 218 Views
Genes & Genomics https://doi.org/10.1007/s13258-020-00987-9
RESEARCH ARTICLE
Trans‑cinnamaldehyde protects C2C12 myoblasts from DNA damage, mitochondrial dysfunction and apoptosis caused by oxidative stress through inhibiting ROS production Yung Hyun Choi1,2 Received: 14 July 2020 / Accepted: 12 August 2020 © The Genetics Society of Korea 2020
Abstract Background Oxidative stress-induced myoblast damage is one of the major causes of skeletal muscle loss associated with inhibition of myogenic differentiation and muscle dysfunction. Trans-cinnamaldehyde (tCA), the most common essential oil constituent in cinnamon, is known to possess strong anti-oxidant activity. However, it has not been determined whether tCA can protect myoblasts from oxidative damage. Objectives The aim of this study was to investigate the protective effect of tCA against oxidative stress-induced damage in mouse myoblast C2C12 cells. Methods To examine the efficacy of tCA to protect against oxidative damage, cell viability, morphological changes, DNA damage, mitochondrial membrane potential (MMP) analysis, reactive oxygen species (ROS) generation, and Western blotting were applied. Results tCA suppressed hydrogen peroxide ( H2O2)-induced growth inhibition and DNA damage by blocking abnormal ROS accumulation. In addition, tCA attenuated apoptosis by suppressing loss of MMP and cytosolic release of cytochrome c, increasing the rate of Bcl-2/Bax expression and reducing the activity of caspase-3 in H2O2-stimulated cells, suggesting that tCA protected C2C12 cells from mitochondria-mediated apoptosis caused by oxidative stress. Conclusion The results showed that tCA may be useful as a potential treatment for the prevention and treatment of various oxidative stress-related muscle disorders in the future. Keywords Trans-cinnamaldehyde · Reactive oxygen species · DNA damage · Apoptosis
Introduction Myoblasts are embryonic precursors of muscle cells formed from tissue-resident stem cells called muscle stem or satellite cells. They undergo a myogenesis process that fuses into multi-nucleated myotubes to differentiate into muscle cells. Myoblasts are one of the most vulnerable organs to oxidative stress, characterized by excessive accumulation of reactive oxygen species (ROS), because they process a large amount of oxygen due to high energy demand (Chang * Yung Hyun Choi [email protected] 1
2
Anti‐Aging Research Center, Dong‐eui University, Busan 47340, Republic of Korea
Department of Biochemistry, Dong‐eui University College of Korean Medicine, Busan 47227, Republic of Korea
and Rudnicki 2014; Sambasivan and Tajbakhsh 2015). In the process of myogenesis, the role of ROS varies by the wide range of cellular responses depending on the level of ROS. ROS regulates various cellular signaling pathways, including muscle differentiation, at moderate levels, but excessive accumulation of ROS is closely related to abnormal myogenesis in response to aging and injury repair (Hansen et al. 2007; Santa-Gonzalez et al. 2016). In addition, enhanced ROS p
Data Loading...
