Table 2.

Inhibitors of M2 polarization in models of pulmonary fibrosis and their anti-fibrotic mechanisms.

Inhibitors	Mechanisms	References
JAK inhibitors	Down-regulate polarization markers (CD86, MHC-II, TLR4) and inflammatory cytokines (CXCL10, IL-6, TNF-α), and restrict the activation of M2 macrophages.	[65]
Nintedanib	Impair the polarization of monocytes towards M2 and reduce the number of M2 macrophages.	[66]
Pirfenidone	Reduce the expression of M2 markers and the release of TGF-β1 from M2 alveolar macrophages and attenuate the proliferation of lung fibroblasts from the culture supernatant of M2 alveolar macrophages.	[67]
Schisandra	Suppress the polarization of AM to M2 macrophages by inhibiting the TGF-β1/Smad pathway.	[68]
Microcystin-LR	Inhibit the endoplasmic reticulum stress response (Accumulation of misfolded proteins in the endoplasmic reticulum. This condition is called endoplasmic reticulum stress. The endoplasmic reticulum stress of macrophages in the lung may be beneficial to the polarization of M2 macrophages [69,70]) mediated by glucose regulatory protein 78 (GRP78).	[71]
Imatinib-loaded gold nanoparticles	Induce apoptosis in lung fibroblasts, inhibit their proliferation and viability and effectively limit IL-8 production, AM viability, and M2 polarization.	[72]

JAK, Janus kinase; MHC-II, MHC class II; TLR4, Toll-like receptor 4; CXCL10, C-X-C motif ligand 10.