Allicin attenuates silica-induced pulmonary fibrosis via Serpinb2/NF-Kappa B pathway

Background Silica-induced pulmonary fibrosis is a debilitating condition with limited therapeutic options. Allicin, a bioactive compound derived from garlic, has shown potential anti-inflammatory and antifibrotic properties. However, its role in silica-induced pulmonary fibrosis remains unexplored. Methods In this study, we employed both in vitro and in vivo models to investigate the effects of allicin on silica-induced pulmonary fibrosis. Human lung epithelial cells (BEAS-2B) and alveolar epithelial cells (A549) were exposed to silica particles, followed by allicin treatment. For in vivo experiments, a murine model of silica-induced pulmonary fibrosis was established, and lentiviral tracheal instillation was employed to validate the impact of Serpinb2 knockdown on fibrotic progression. Fibrosis and ferroptosis markers, including GSH/GSSG, MDA and hydroxyproline content, were assessed. Molecular mechanisms were evaluated using Western blot, RT-PCR, and Immunofluorescence to analyze Serpinb2 expression and NF-κB pathway activation. Results Allicin can alleviate ferroptosis and pulmonary fibrosis induced by silica. In addition, Serpinb2 is upregulated under the induction of silicon dioxide. Inhibiting Serpinb2 can alleviate ferroptosis and pulmonary fibrosis induced by silicon dioxide. Meanwhile, the addition of allicin can inhibit Serpinb2 and thereby exert the same effect. NF-kB functions as a downstream pathway of Serpinb2. The addition of allicin can inhibit Serpinb2 and thereby suppress the NF-kB pathway, thereby exerting its inhibitory effect on ferroptosis and pulmonary fibrosis. Conclusion This study demonstrates that allicin attenuates silica-induced pulmonary fibrosis by modulating Serpinb2/NF-κB pathway via inhibiting ferroptosis. These results highlight the therapeutic potential of allicin in treating pulmonary fibrosis and provide a novel mechanistic insight into its antifibrotic effects.