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Description
Ethanol is highly addictive and accounts for 5% of deaths worldwide. Ethanol consumption is known for its physical effects such as nausea, loss of motor control, and vomiting, but more importantly, ethanol metabolism is attributed to the formation of toxic molecules like acetaldehydes, oxidative stressors, and proinflammatory cytokines. The toxicity of ethanol causes damage to the vital organs, most notably the liver, and can lead to a myriad of health complications such as cirrhosis and cancer. Dihydromyricetin (DHM), a bioactive flavonoid isolated from Hovenia dulcis, has been shown to counteract ethanol intoxication and diminish the toxic effects of ethanol. In previous research, DHM has been shown to not only have anti-ethanol properties, but also antioxidant, anti-inflammatory, anti-microbial, and anti-diabetic behavior. Although DHM appears to be beneficial, many of the mechanisms associated with its effects are unknown and need to be explored further. In this study, untargeted metabolome profiling was performed using liquid chromatography coupled with high-resolution mass spectrometry and bioinformatics to determine the unique metabolites that were dysregulated in the livers, kidneys, and spleens of DHM-treated mice. Alterations in small molecule metabolites can indicate changes in metabolic activity, protein function, and gene expression. Together these changes can reveal how DHM mediates ethanol’s toxicity. The data suggest that DHM has a significant impact, as many key metabolites and metabolic pathways were dysregulated compared to mice that were only given ethanol. Purine metabolism, fatty acid oxidation, prostaglandin synthesis, glutathione production, and amino acid functioning were altered in the DHM treated mice compared to the ethanol-only control. Our results suggest that DHM initiates AMPK inhibition of NF-κB and may affect ethanol’s behavior effects through changes in amino acid signaling. These results indicate that DHM has a potential for therapeutic applications.
