An Investigation of PFOS-Induced Liver Injury in Quail and the Intervening Role of Chlorogenic Acid Based on Network Toxicology

Perfluorooctanesulfonate (PFOS), as an environmental pollutant that can cause abnormal lipid metabolism in the liver of humans and livestock, has currently posed a threat to global environmental hygiene. This study employed network toxicology and network pharmacology methods to conduct a comprehensive analysis of the hepatotoxicity mechanism of PFOS and the hepatoprotective mechanism of chlorogenic acid (CGA), and further validated the lipid metabolism abnormalities and lipid phagocytosis mechanisms of PFOS. The results of the joint analysis indicated that the Estrogen Receptor (ESR) pathway was the common action pathway of PFOS and CGA. Further validation revealed that PFOS activates the ESR and nuclear factor kappa-B (NF-κB) pathways, increases lipid accumulation, and enhances hepatic lipophagocytosis; whereas CGA intervention suppresses the ESR pathway, alleviates PFOS-induced lipid accumulation, inhibits lipid phagocytosis, and thereby mitigates PFOS-induced hepatic tissue damage. This study laid a theoretical foundation for CGA as a potential hepatoprotective agent.