Our examination of the role of macrophages in the pathogenesis of IPF revealed HG2’s notable ability to inhibit M2 macrophage polarization during BLM-induced pulmonary fibrosis and effectively suppress LPS or LPS combined with IFN-γ-induced macrophage inflammation and M1-type polarization. This evidence concerns the gene PKD1P2 and idiopathic interstitial pneumonia.