Li-Ginseng powder protects against alcohol-induced liver injury by promoting acetaldehyde clearance and cellular homeostasis

Nov 21, 2025Journal of ginseng research

Li-Ginseng powder may protect the liver from alcohol damage by helping remove harmful acetaldehyde and maintaining cell balance

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Abstract

Ethanol exposure significantly elevated serum levels of liver enzymes and other markers, while Li-Ginseng Powder (LGP) reversed these changes.

Daily oral administration of ethanol (2400 mg/kg) in mice led to increased liver injury markers, including aspartate aminotransferase and alanine aminotransferase.
LGP pre-treatment restored antioxidant levels and alleviated liver damage and fat accumulation in ethanol-exposed mice.
In liver cells exposed to ethanol, LGP improved the activity of enzymes responsible for detoxifying alcohol and its byproducts.
LGP reduced oxidative stress markers and preserved mitochondrial function, contributing to liver cell health.
These results indicate that LGP may protect against alcohol-induced liver injury through multiple mechanisms.

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BACKGROUND: Chronic and excessive alcohol consumption is a primary driver of alcohol-associated liver disease (ALD), a global health challenge with limited treatment options. Panax ginseng Meyer exhibits various pharmacological activities, including antioxidant and anti-inflammatory effects. However, its efficacy in preventing alcohol-induced liver injury remains limited, necessitating further optimization and investigation.

METHODS: This study evaluated the hepatoprotective effects of Li-Ginseng Powder (LGP), a ginseng preparation enriched in rare ginsenosides, using a murine model of ALD and ethanol-exposed human hepatic L-02 cells. ALD was induced in C57BL/6 mice via daily oral ethanol administration (2400 mg/kg). Serum and liver biochemical markers were measured, and histological changes were assessed using H&E and Oil Red O staining. In vitro assays examined the effects of LGP on ethanol-metabolizing enzyme activity, oxidative stress, mitochondrial integrity, and autophagy.

RESULTS: Ethanol exposure significantly elevated serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, low-density lipoprotein, and cholesterol, as well as hepatic triglycerides and malondialdehyde, while markedly decreasing hepatic levels of reduced glutathione and superoxide dismutase. LGP pre-treatment effectively reversed all these alterations, restored antioxidant capacity, and alleviated histological damage and lipid accumulation to near normal levels. In L-02 cells, LGP significantly enhanced alcohol dehydrogenase and aldehyde dehydrogenase activities, facilitated ethanol and acetaldehyde detoxification, reduced reactive oxygen species levels, preserved mitochondrial membrane potential, and promoted autophagy.

CONCLUSION: LGP confers comprehensive hepatoprotection against alcohol-induced liver injury by significantly enhancing ethanol catabolism, enhancing antioxidant defenses, and activating autophagy. These findings suggest its therapeutic potential in the management of ALD.

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Li-Ginseng powder protects against alcohol-induced liver injury by promoting acetaldehyde clearance and cellular homeostasis

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