Ent -Peniciherqueinone Suppresses Acetaldehyde-Induced Cytotoxicity and Oxidative Stress by Inducing ALDH and Suppressing MAPK Signaling

Studies on ethanol-induced stress and acetaldehyde toxicity are actively being conducted, owing to an increase in alcohol consumption in modern society. In this study, -peniciherqueinone (EPQ) isolated from a Hawaiian volcanic soil-associated fungus FT729 was found to reduce the acetaldehyde-induced...

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Published in:Pharmaceutics 2020-12, Vol.12 (12), p.1229
Main Authors: Oh, Taehoon, Kwon, Mincheol, Yu, Jae Sik, Jang, Mina, Kim, Gun-Hee, Kim, Ki Hyun, Ko, Sung-Kyun, Ahn, Jong Seog
Format: Article
Language:English
Subjects:
acetaldehyde
Alcohol
anti-oxidation
Antibodies
Apoptosis
Chromatography
Cytotoxicity
Dehydrogenases
ent-peniciherqueinone
Ethanol
Kinases
Liver
Oxidative stress
Solvents
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Summary:Studies on ethanol-induced stress and acetaldehyde toxicity are actively being conducted, owing to an increase in alcohol consumption in modern society. In this study, -peniciherqueinone (EPQ) isolated from a Hawaiian volcanic soil-associated fungus FT729 was found to reduce the acetaldehyde-induced cytotoxicity and oxidative stress in PC12 cells. EPQ increased cell viability in the presence of acetaldehyde-induced cytotoxicity in PC12 cells. In addition, EPQ reduced cellular reactive oxygen species (ROS) levels and restored acetaldehyde-mediated disruption of mitochondrial membrane potential. Western blot analyses revealed that EPQ treatment increased protein levels of ROS-scavenging heme oxygenase-1 and superoxide dismutase, as well as the levels of aldehyde dehydrogenase (ALDH) 1, ALDH2, and ALDH3, under acetaldehyde-induced cellular stress. Finally, EPQ reduced acetaldehyde-induced phosphorylation of p38 and c-Jun N-terminal kinase, which are associated with ROS-induced oxidative stress. Therefore, our results demonstrated that EPQ prevents cellular oxidative stress caused by acetaldehyde and functions as a potent agent to suppress hangover symptoms and alcohol-related stress.
ISSN:1999-4923
1999-4923
DOI:10.3390/pharmaceutics12121229