Lecithin exerts direct lipid-lowering and antioxidant cytoprotective effects in vitro: implications for laying hen fatty liver hemorrhagic syndrome.

BACKGROUND: Fatty liver hemorrhagic syndrome (FLHS) is a prevalent metabolic disorder in laying hens that severely compromises physiological health and egg production. Lecithin, a vital phospholipid complex, is known for its lipotropic and cytoprotective properties; however, whether its preventive effects against FLHS act directly on the liver or rely on systemic shifts remains elusive. This study aimed to investigate the direct cytoprotective role and molecular mechanisms of lecithin using an isolated cell-based model of FLHS.

METHODS: An in vitro steatosis model was established by treating Leghorn male hepatoma (LMH) cells with exogenous free fatty acids (FFAs). Lipid accumulation and redox status were assessed by quantifying intracellular triglycerides (TG), superoxide dismutase (SOD) activity, and reduced glutathione (GSH) content. The expression of key lipogenic genes, including acetyl-CoA carboxylase (ACC) and stearoyl-CoA desaturase 1 (SCD1), was validated via qPCR. Furthermore, transcriptomic sequencing (RNA-seq) was integrated with bioinformatic analysis to identify differentially expressed genes (DEGs) and functional signaling pathways.

RESULTS: Lecithin supplementation significantly attenuated FFAs-induced TG accumulation (p < 0.05) and restored cellular redox homeostasis by increasing SOD activity and GSH levels (p < 0.05). In normal hepatocytes, lecithin downregulated the expression of ACC and SCD1 (p < 0.01). Under steatotic conditions, lecithin specifically suppressed SCD1 mRNA levels (p < 0.05). Transcriptomic profiling identified 397 DEGs between the FFA and FFA + lecithin groups. Functional enrichment analysis revealed that these DEGs were primarily involved in oxidoreductase activity and the arachidonic acid metabolism pathway, particularly focusing on cyclooxygenase and prostaglandin-endoperoxide synthase activities.

CONCLUSION: This study demonstrates that lecithin possesses the capacity to directly protect hepatocytes by attenuating lipid accumulation and enhancing antioxidant defenses, suggesting that its preventive role against FLHS is driven, at least in part, by direct hepatic action rather than relying solely on systemic metabolism. Furthermore, we hypothesize that lecithin may potentially offer additional protection through indirect anti-inflammatory actions. These findings provide a robust theoretical foundation for elucidating the direct hepatoprotective mechanisms of lecithin, contributing to a clearer understanding of its role in FLHS prevention and supporting its scientific dietary supplementation in laying hens, particularly during the peak and late laying periods.