Allicin attenuates silica-induced pulmonary fibrosis by targeting the Serpinb2/NF-κB pathway

Silica-induced pulmonary fibrosis (silicosis) is a severe, progressive, and often fatal interstitial lung disease, primarily an occupational hazard, with very limited effective therapeutic options. Current treatments often only manage symptoms or slow progression, failing to halt the underlying fibrotic process. Allicin, a natural organosulfur compound from garlic, has demonstrated promising anti-inflammatory and antifibrotic properties in various contexts. This study investigates allicin's potential to address the unmet need in silicosis by exploring its specific mechanistic role, particularly concerning cellular ferroptosis and key signaling pathways.

Researchers investigated allicin's effects in both in vitro and in vivo models. Human lung epithelial cells (BEAS-2B) and alveolar epithelial cells (A549) were exposed to silica particles, followed by allicin treatment. A murine model of silica-induced pulmonary fibrosis was established, and lentiviral tracheal instillation validated Serpinb2 knockdown's impact on fibrosis. Fibrosis and ferroptosis markers, including GSH/GSSG ratio, MDA content, and hydroxyproline levels, were assessed. Molecular mechanisms were evaluated using Western blot, RT-PCR, and Immunofluorescence to analyze Serpinb2 expression and NF-κB pathway activation.