Pakistan Journal of Pharmaceutical Sciences

Abstract: Background: Alcoholic liver disease (ALD) poses a significant global health challenge by causing progressive damage due to excessive alcohol consumption, highlighting the urgent need for effective treatments. Jin Ge Fang (JGF) is a traditional formulation whose potential hepatoprotective mechanism remains to be fully elucidated. Objectives: This study aimed to investigate the protective effects of JGF on ALD and explore its regulatory roles in oxidative stress, inflammatory cascades, and the Toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-?B) pathway. Methods: An ethanol-induced ALD rat model was established and assessed histopathologically. Serum levels of hepatic function markers [aspartate transaminase (AST) and alanine transaminase (ALT)] and oxidative stress indicators [malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px)] were measured. Inflammatory cytokines [tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6), and interleukin-1? (IL-1?)] were quantified using enzyme-linked immunosorbent assay (ELISA). Protein expression related to the TLR4/NF-?B pathway was analyzed by Western blotting. Results: JGF treatment significantly improved liver histology, reducing steatosis and inflammatory infiltration. It markedly decreased serum AST and ALT activities, suppressed lipid peroxidation (as evidenced by reduced MDA levels), and enhanced endogenous antioxidant defenses (elevated SOD and GSH-Px activities). Furthermore, JGF significantly inhibited the release of pro-inflammatory cytokines (TNF-?, IL-6, and IL-1?) and downregulated the protein expression of key mediators in the TLR4/NF-?B signaling pathway. Conclusion: JGF demonstrates significant hepatoprotective effects against ALD. Its benefits are likely mediated through a dual action of ameliorating oxidative damage and suppressing inflammatory activation, potentially via inhibition of the TLR4/NF-?B signaling cascade.