ArticleMarine drugs2015
Ecklonia cava Polyphenol Has a Protective Effect against Ethanol-Induced Liver Injury in a Cyclic AMP-Dependent Manner.
Article in Marine drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Modulation of ER Stress via cAMP Signaling: Protective Role of Rolipram in Paracetamol-Induced Liver Injury.Chemical research in toxicology · 2026Article
- Article
- Aqueous extract ofNutrition research and practice · 2023Article
- Polydatin: A Critical Promising Natural Agent for Liver Protection via Antioxidative Stress.Oxidative medicine and cellular longevity · 2022Review
- Role of cAMP and phosphodiesterase signaling in liver health and disease.Cellular signalling · 2018Review
- Anti-inflammatory and hepatoprotective effects of exopolysaccharides isolated from Pleurotus geesteranus on alcohol-induced liver injury.Scientific reports · 2018Article
- The Potential and Action Mechanism of Polyphenols in the Treatment of Liver Diseases.Oxidative medicine and cellular longevity · 2018Review
- Recent advances in pharmacological research on Ecklonia species: a review.Archives of pharmacal research · 2017Review
- Polydatin Protects Rat Liver against Ethanol-Induced Injury: Involvement of CYP2E1/ROS/Nrf2 and TLR4/NF-κB p65 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Melatonin Improves Waterlogging Tolerance ofFrontiers in plant science · 2017Article
- Protective Effects of Hydrolyzed Nucleoproteins from Salmon Milt against Ethanol-Induced Liver Injury in Rats.Marine drugs · 2016Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we showed that Ecklonia cava polyphenol (ECP) treatment suppressed ethanol-induced increases in hepatocyte death by scavenging intracellular reactive oxygen species (ROS) and maintaining intracellular glutathione levels. Here, we examined the effects of ECP on the activities of alcohol-metabolizing enzymes and their regulating mechanisms in ethanol-treated hepatocytes. Isolated hepatocytes were incubated with or without 100 mM ethanol. ECP was dissolved in dimethylsulfoxide. ECP was added to cultured cells that had been incubated with or without ethanol. The cells were incubated for 0-24 h. In cultured hepatocytes, the ECP treatment with ethanol inhibited cytochrome P450 2E1 (CYP2E1) expression and activity, which is related to the production of ROS when large quantities of ethanol are oxidized. On the other hand, ECP treatment with ethanol increased the activity of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. These changes in activities of CYP2E1 and ADH were suppressed by treatment with H89, an inhibitor of protein kinase A. ECP treatment with ethanol enhanced cyclic AMP concentrations compared with those of control cells. ECP may be a candidate for preventing ethanol-induced liver injury via regulating alcohol metabolic enzymes in a cyclic AMP-dependent manner.
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