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

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.