Yung Hyun Choi1,2. 1. Anti-Aging Research Center, Dong-eui University, Busan, 47340, Republic of Korea. choiyh@deu.ac.kr. 2. Department of Biochemistry, Dong-eui University College of Korean Medicine, Busan, 47227, Republic of Korea. choiyh@deu.ac.kr.
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.
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.
Entities:
Keywords:
Apoptosis; DNA damage; Reactive oxygen species; Trans-cinnamaldehyde