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Ginsenoside‐Free Molecules from Steam‐Dried Ginseng Berry Promote Ethanol Metabolism: An Alternative Choice for an Alcohol Hangover

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AbstractEthanol metabolism produces harmful compounds that contribute to liver damage and cause an alcohol hangover. The intermediate metabolite acetaldehyde is responsible for alcohol hangover and CYP2E1‐induced reactive oxygen species damage liver tissues. In this study, we examined whether ginsenoside‐free molecules (GFMs) from steam‐dried ginseng berries promote ethanol metabolism and scavenge free radicals by stimulating primary enzymes (alcohol dehydrogenase, aldehyde dehydrogenase, CYP2E1, and catalase) and antioxidant effects using in vitro and in vivo models. The results revealed that GFM effectively scavenged 2,2‐diphenyl‐1‐picrylhydrazyl hydrate radicals and hydroxyl radicals. Notably, GFM significantly enhanced the expression of primary enzymes within 2 h in HepG2 cells. GFM clearly removed the consumed ethanol and significantly reduced the level of acetaldehyde as well as enhancement of primary gene expression in BALB/c mice. Moreover, GFM successfully protected HepG2 cells from ethanol attack. Of the major components identified in GFM, it was believed that linoleic acid was the most active ingredient. Based on these findings, we conclude that GFM holds promise for use as a new candidate for ethanol metabolism and as an antihangover agent.
Title: Ginsenoside‐Free Molecules from Steam‐Dried Ginseng Berry Promote Ethanol Metabolism: An Alternative Choice for an Alcohol Hangover
Description:
AbstractEthanol metabolism produces harmful compounds that contribute to liver damage and cause an alcohol hangover.
The intermediate metabolite acetaldehyde is responsible for alcohol hangover and CYP2E1‐induced reactive oxygen species damage liver tissues.
In this study, we examined whether ginsenoside‐free molecules (GFMs) from steam‐dried ginseng berries promote ethanol metabolism and scavenge free radicals by stimulating primary enzymes (alcohol dehydrogenase, aldehyde dehydrogenase, CYP2E1, and catalase) and antioxidant effects using in vitro and in vivo models.
The results revealed that GFM effectively scavenged 2,2‐diphenyl‐1‐picrylhydrazyl hydrate radicals and hydroxyl radicals.
Notably, GFM significantly enhanced the expression of primary enzymes within 2 h in HepG2 cells.
GFM clearly removed the consumed ethanol and significantly reduced the level of acetaldehyde as well as enhancement of primary gene expression in BALB/c mice.
Moreover, GFM successfully protected HepG2 cells from ethanol attack.
Of the major components identified in GFM, it was believed that linoleic acid was the most active ingredient.
Based on these findings, we conclude that GFM holds promise for use as a new candidate for ethanol metabolism and as an antihangover agent.

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