Ent-peniciherqueinone suppresses acetaldehyde-induced cytotoxicity and oxidative stress by inducing aldh and suppressing mapk signaling

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Abstract

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, ent-peniciherqueinone (EPQ) isolated from a Hawaiian volcanic soil-associated fungus Penicillium herquei 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.

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Oh, T., Kwon, M., Yu, J. S., Jang, M., Kim, G. H., Kim, K. H., … Ahn, J. S. (2020). Ent-peniciherqueinone suppresses acetaldehyde-induced cytotoxicity and oxidative stress by inducing aldh and suppressing mapk signaling. Pharmaceutics, 12(12), 1–12. https://doi.org/10.3390/pharmaceutics12121229

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