잠시만 기다려 주세요. 로딩중입니다.

Indole-6-carboxaldehyde prevents oxidative stress-induced mitochondrial dysfunction, DNA damage and apoptosis in C2C12 skeletal myoblasts by regulating the ROS-AMPK signaling pathway

Molecular & Cellular Toxicology 2020년 16권 4호 p.455 ~ 467
박철, 이혜숙, 박신형, 홍수현, 송경섭, 차희재, 김기영, 장영채, 김석만, 김희수, 최영현,
소속 상세정보
박철 ( Park Cheol ) - Dong-Eui University College of Liberal Studies Division of Basic Sciences
이혜숙 ( Lee Hye-Sook ) - Dong-Eui University Anti-Aging Research Center
박신형 ( Park Shin-Hyung ) - Dong-Eui University College of Korean Medicine Department of Pathology
홍수현 ( Hong Su-Hyun ) - Dong-Eui University Anti-Aging Research Center
송경섭 ( Song Kyoung-Seob ) - Kosin University College of Medicine Department of Cell Biology
차희재 ( Cha Hee-Jae ) - Kosin University College of Medicine Department of Parasitology and Genetics
김기영 ( Kim Gi-Young ) - Jeju National University School of Marine Biomedical Sciences Department of Marine Life Sciences
장영채 ( Chang Young-Chae ) - Catholic University of Daegu School of Medicine Department of Medicine
김석만 ( Kim Suhk-Mann ) - Pusan National University College of Natural Sciences Department of Chemistry
김희수 ( Kim Heui-Soo ) - Pusan National University College of Natural Sciences Department of Biological Sciences
최영현 ( Choi Yung-Hyun ) - Dong-Eui University College of Korean Medicine Department of Biochemistry

Abstract


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.

키워드

Indole-6-carboxaldehyde; Oxidative stress; DNA damage; Apoptosis; AMPK

원문 및 링크아웃 정보

등재저널 정보