Wenjing He, Binbin Zhang, Siwei Li, Yuanyuan Qian
Background: Alcoholic liver disease (ALD) remains a major global health burden, and effective therapeutic options are limited. Quercetin, a dietary flavonoid with antioxidant and anti-inflammatory properties, has shown hepatoprotective potential, but its mechanisms in acute alcohol-induced liver injury require clarification. Methods: Fifty male BALB/c mice were randomly divided into five groups (n = 10/group): control (CG), model (MG), low-dose quercetin (LQ, 50 mg/kg), high-dose quercetin (HQ, 100 mg/kg), and oyster soybean carnitine mice in the oyster soybean carnitine group (OG) were administered oyster soybean carnitine at a volume of 20 mL/kg.(OG, 20 mL/kg). All treatments were administered orally once daily for 14 days. Acute alcohol injury was induced on Day 14 using 52% (v/v) ethanol. Behavioral intoxication indices, serum biochemistry, liver oxidative stress markers, inflammatory cytokines, histopathology, lipid accumulation, and the expression of lipid-metabolismrelated genes and proteins (FAS, SCD1, ACC1, CPT1, PGC-1α, PPARα) were assessed. Results: HQ significantly prolonged alcohol tolerance time (P < 0.01) and shortened sober-up time (P < 0.01). HQ markedly reduced serum AST, ALT, TG, FFA, and glycerol levels (P < 0.01). Quercetin also lowered hepatic TG, TNF-α, and IL-6 and increased SOD, GSH, and CAT activities. Histological and Oil Red O staining confirmed reduced steatosis. Mechanistically, quercetin downregulated hepatic FAS, SCD1, and ACC1 while upregulating CPT1, PGC-1α, and PPARα at both mRNA and protein levels. Conclusion: Quercetin exerts hepatoprotective effects against acute alcohol-induced liver injury through coordinated regulation of lipid metabolism, oxidative stress, and inflammatory responses.The study did not include a quercetin-only group or measure blood ethanol levels, which should be addressed in future work.These findings support the potential of quercetin as a natural candidate for preventing alcohol-related hepatic injury.