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KMID : 1034820200160040455
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Molecular & Cellular Toxicology
2020 Volume.16 No. 4 p.455 ~ p.467
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Indole-6-carboxaldehyde prevents oxidative stress-induced mitochondrial dysfunction, DNA damage and apoptosis in C2C12 skeletal myoblasts by regulating the ROS-AMPK signaling pathway
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Park Cheol
Lee Hye-Sook
Park Shin-Hyung
Hong Su-Hyun
Song Kyoung-Seob
Cha Hee-Jae
Kim Gi-Young
Chang Young-Chae
Kim Suhk-Mann
Kim Heui-Soo
Choi Yung-Hyun
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Abstract
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Background: Indole-6-carboxaldehyde (I6CA), a natural indole derivative derived from the brown algae Sargassum thunbergii (Mertens) Kuntze, is known to have several pharmacological activities. However, the antioxidant effects of I6CA have not been identified.
Objective: The study aimed to investigate the protective effect of I6CA and its underlying mechanism against oxidative stress-induced damage in C2C12 mouse skeletal myoblasts.
Results: The findings revealed that pretreatment with I6CA protected hydrogen peroxide (H2O2)-induced cytotoxicity and DNA damage through blockage of intracellular reactive oxygen species (ROS) generation. I6CA also significantly suppressed C2C12 cells against H2O2-induced apoptosis by preventing loss of mitochondrial membrane potential and cytosolic release of cytochrome c, decreasing the rate of Bax/Bcl-2 expression and reducing the activity of caspases. In addition, I6CA markedly attenuated the decrease in ATP content induced by H2O2 and restored H2O2-induced activation of AMP-activated protein kinase (AMPK). However, the cytoprotective effects of I6CA against H2O2 were eliminated by compound C, a specific AMPK signaling blocker.
Conclusion: The current results indicate that I6CA was able to protect C2C12 myoblast DNA damage and apoptosis from oxidative stress by at least preserving mitochondrial homeostasis mediated through the ROS-AMPK signaling pathway.
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KEYWORD
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Indole-6-carboxaldehyde, Oxidative stress, DNA damage, Apoptosis, AMPK
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