Page 22 - F. Cell biology

[F. Cell biology-14]

Indole-6-carboxaldehyde prevents oxidative stress-induced

DNA damage and apoptosis in C2C12 skeletal myoblasts by

regulating the ROS-AMPK signaling pathway

Cheol Park¹, Yung Hyun Choi²˙³˙*

¹Basic Sciences, College of Liberal Studies, Dong-eui University, Busan 47340, Republic of Korea, ²Biochemistry,

Dong-eui University College of Korean Medicine, Busan 47227, Republic of Korea, ³Anti-Aging Research Center,
Dong-eui University, Busan 47340, Republic of Korea

Myoblast damage due to oxidative stress is one of the main causes of skeletal muscle loss associated with the

inhibition of myopic differentiation and induction of muscle damage. Indole-6-carboxaldehyde (I6CA), a natural
indole derivative derived from the brown algae Sargassum thunbergii, is known to have several pharmacological

activities. However, the antioxidative effects of I6CA have not been identified. In this study, we investigated that the
protective effect of I6CA and its underlying mechanism in vitro using hydrogen peroxide (H2O2)-induced oxidative

stress in a C2C12 mouse skeletal myoblast. The findings revealed that pretreatment with I6CA protected H2O2-
induced cytotoxicity and DNA damage by blockage of ROS generation. Further studies have shown that I6CA

suppressed C2C12 cells against H2O2-induced apoptosis by preventing loss of mitochondrial membrane potential.
I6CA attenuated H2O2-induced activation of AMPK and ATP content. Additionally, the cytoprotective effects of I6CA

against H2O2 were eliminated by compound C, a specific AMPK blocker. Collectively, the current results indicate
that I6CA was able to protect C2C12 cells DNA damage and apoptosis from oxidative stress by at least preserving

mitochondrial homeostasis mediated through the ROS-AMPK signaling pathway.