Background Silicosis is a progressive pulmonary fibrotic disease caused by long-term inhalation of silica (SiO₂) dust, and abnormal fibroblast activation is a central pathological mechanism. Galectin 3 (LGALS3) plays a significant role in fibrosis across multiple organs; however, its specific molecular mechanism in SiO₂-induced pulmonary fibrosis remains unclear. Objective To investigate the role of LGALS3 in silica (SiO₂) induced pulmonary fibrosis and its potential molecular mechanisms. Methods Differentially expressed genes in mouse lung fibroblasts treated with SiO₂ for 56 d were analysed using the GSE183682 single-cell RNA sequencing dataset, followed by pathway enrichment analysis. A mouse model of pulmonary fibrosis was established by intratracheal instillation of SiO₂ suspension (50 mg·mL⁻¹, 100 μL). Lung index, hydroxyproline content, and histopathological changes (HE staining) were assessed. Western blot and immunofluorescence staining were used to evaluate the expression of LGALS3, MAPK pathway proteins, and fibrosis markers [collagen type I alpha 1 chain (COL1A1) and α-smooth muscle actin (ACTA2)]. Results Single-cell RNA sequencing analysis identified 53 differentially expressed genes in fibroblasts, and Lgals3 was significantly upregulated in the SiO₂ group. SiO₂ exposure successfully induced pulmonary fibrosis in mice, as indicated by weight loss, elevated hydroxyproline content, alveolar structural disruption, and collagen deposition. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that Lgals3-associated genes were enriched in Toll-like receptor/chemokine signaling pathways. After SiO₂ exposure, LGALS3 expression was increased in fibrotic lung tissue and co-localized with ACTA2, an activated fibroblast and myofibroblast marker. This was accompanied by activation of the MAPK signaling pathway. Conclusion LGALS3 may be involved in fibroblast activation and collagen deposition, potentially through activation of the MAPK signalling pathway. These findings suggest that LGALS3 may represent a potential regulatory target in SiO₂-induced pulmonary fibrosis.

Objective To explore the significance of the toxicity mechanism of butyl benzyl phthalate(BBP)in prevention and treatment of pulmonary fibrosis.Methods In this study,we used network toxicology combined with molecular docking technology to screen the targets of BBP and those related to pulmonary fibrosis through PubChem,GeneCards and other databases,and analyzed the intersecting genes by using a Wayne diagram.Protein-protein interaction networks were constructed to screen the core targets,and the pathway mechanisms were revealed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Finally,molecular docking using AutoDock was performed to verify the binding patterns of core targets and BBP.Results A total of 91 potential targets of BBP-induced lung fibrosis were screened,among which PTGS2 and CYP3A4 were the core targets(binding energies of-1.84 kcal/mol and-1.68 kcal/mol,respectively).Enrichment analysis showed that BBP regulated the fibrosis process through G protein-coupled receptor signaling pathway,calcium signaling pathway and cyclic adenosine monophosphate signaling pathway.Molecular docking confirmed that BBP was stably bound to the core target through hydrogen bonding and hydrophobic interaction.Conclusion This study provides preliminary insights into the molecular mechanism of BBP-induced pulmonary fibrosis through network toxicology,and PTGS2 and CYP3A4 may play key roles in BBP-induced pulmonary fibrosis,which provides a novel reference for the exploration of the mechanism of toxicant-disease association.

Objective To explore the significance of the toxicity mechanism of butyl benzyl phthalate(BBP)in prevention and treatment of pulmonary fibrosis.Methods In this study,we used network toxicology combined with molecular docking technology to screen the targets of BBP and those related to pulmonary fibrosis through PubChem,GeneCards and other databases,and analyzed the intersecting genes by using a Wayne diagram.Protein-protein interaction networks were constructed to screen the core targets,and the pathway mechanisms were revealed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Finally,molecular docking using AutoDock was performed to verify the binding patterns of core targets and BBP.Results A total of 91 potential targets of BBP-induced lung fibrosis were screened,among which PTGS2 and CYP3A4 were the core targets(binding energies of-1.84 kcal/mol and-1.68 kcal/mol,respectively).Enrichment analysis showed that BBP regulated the fibrosis process through G protein-coupled receptor signaling pathway,calcium signaling pathway and cyclic adenosine monophosphate signaling pathway.Molecular docking confirmed that BBP was stably bound to the core target through hydrogen bonding and hydrophobic interaction.Conclusion This study provides preliminary insights into the molecular mechanism of BBP-induced pulmonary fibrosis through network toxicology,and PTGS2 and CYP3A4 may play key roles in BBP-induced pulmonary fibrosis,which provides a novel reference for the exploration of the mechanism of toxicant-disease association.