Biotechnology and Bioprocess Engineering 2022; 27(2): 171-182  
Protection of Oxidative Stress-induced DNA Damage and Apoptosis by Rosmarinic Acid in Murine Myoblast C2C12 Cells
Moon-Jin Jeong, Do-Seon Lim, Sung Ok Kim, Cheol Park, Sun-Hee Leem, Hyesook Lee, Gi-Yung Kim, Soon-Jeong Jeong, and Yung Hyun Choi
Moon-Jin Jeong
Department of Oral Histology and Developmental Biology, School of Dentistry, Chosun University, Gwangju 61452, Korea
Do-Seon Lim
Department of Dental Hygiene, Graduate School of Public Health Science, Eulji University, Seongnam 13135, Korea
Sung Ok Kim
Department of Food Science and Biotechnology, College of Engineering, Kyungsung University, Busan 48434, Korea
Cheol Park
Division of Basic Sciences, College of Liberal Studies, Dong-eui University, Busan 47340, Korea
Sun-Hee Leem
Department of Biological Science, Dong-A University, Busan 49315, Korea Department of Health Sciences, The Graduated of Dong-A University, Busan 49315, Korea
Hyesook Lee, Yung Hyun Choi*
Anti-Aging Research Center, Dong-eui University, Busan 47340, Korea Department of Biochemistry, Dong-eui University College of Korean Medicine, Busan 47227, Korea
Tel: +82-51-890-3319; Fax: +82-51-890-3333
E-mail: choiyh@deu.ac.kr
Gi-Yung Kim
Department of Marine Life Science, Jeju National University, Jeju 63243, Korea
Soon-Jeong Jeong*
Department of Dental Hygiene & Institute of Basic Science for Well- Aging, Youngsan University, Yangsan 50510, Korea
Tel: +82-55-380-9453; Fax: +82-55-380-9305
E-mail: jeongsj@ysu.ac.kr
Moon-Jin Jeong and Do-Seon Lim contributed equally to this work.
Received: August 31, 2021; Revised: September 30, 2021; Accepted: September 30, 2021; Published online: April 30, 2022.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Rosmarinic acid (RA) is a naturally occurring polyphenolic compound that has been applied as a therapeutic antioxidant. However, its action mechanism in muscle cells remains unclear. The objective of the current study was to explore the protective effect of RA against DNA damage and apoptotic cell death caused by hydrogen peroxide (H2O2) in mouse C2C12 myoblast cells and clarify related signaling pathway. Our results showed that pretreatment with RA significantly improved cell viability, inhibited apoptosis, and suppressed the generation of reactive oxygen species (ROS) in H2O2-treated C2C12 cells. Additionally, DNA damage triggered by H2O2 was abrogated by RA pretreatment. Moreover, H2O2-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential and adenosine triphosphate content, up-regulation of Bax, down-regulation of Bcl-2, and cytosolic release of cytochrome c, were reduced in the presence of RA. RA also attenuated H2O2-induced activation of caspase-9 and caspase-3, which was associated with the ability of RA to block the degradation of poly (ADP-ribose) polymerase. Furthermore, RA dramatically promoted nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its phosphorylation in the presence of H2O2 with concomitant upregulation of heme oxygenase-1 (HO-1) expression, a major downstream factor of Nrf2. Taken together, these results suggest that RA could protect C2C12 myoblasts from H2O2-induced damage by maintaining mitochondrial function while eliminating ROS along with activation of the Nrf2/HO-1 antioxidant pathway, indicating that RA may be a potential therapeutic candidate to treat oxidative stress-mediated injury.
Keywords: rosmarinic acid, reactive oxygen species, DNA damage, apoptosis, factor erythroid 2-related factor 2/ heme oxygenase-1


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