Table 4.
Biological materials improving OA pain through promotion of macrophage M2 polarization.
| Biological Materials | Mechanism of Action | Route of Administration | Target Site |
|---|---|---|---|
| MJN110 (a kind of MAGL inhibitor) [101] | Promoting increased expression of PINK1 and Parkin in M1 macrophages to induce mitochondrial autophagy. | Intraperitoneal injection | Joint |
| BTZ@PTK (co-assembly of bortezomib and an amphiphilic copolymer with ROS-cleaved thioketal linkages) [102] | Clearing ROS within the joints, and inhibiting the JAK/STAT signaling pathway in M1 macrophages, thus suppressing M1 polarization of macrophages. | Intra-articular injection | Joint |
| TissueGene-C (a combination of human allogeneic chondrocytes and irradiated GP2-293 cells overexpressing TGF-β1) [103] | Inducing an increase in intra-articular levels of IL-10 and TGF-β1 to promote M2 polarization of macrophages. | Intra-articular injection | Joint |
| Neonatal umbilical cord blood mesenchymal stem cells [104] | The secretion of PTX-3 acts on macrophages to induce M2 phenotype. | Intra-articular injection | Joint |
| Tyrosine hydroxylase-positive cells derived from bone marrow stem cells [105] | The secretion of IL-4 induces M2 polarization of macrophages and catecholamines to exert anti-inflammatory effects. | Intravenous injection | DRG |
| M2 macrophage-derived exosomes miR-26 b-5p [106] | Suppressing the expression of TLR3 on macrophages to inhibit M1 polarization, while promoting the expression of CD206 on their surface to facilitate the transition to M2 type. | Intra-articular injection | Joint |
| Membrane vesicles from Lactobacillus johnsonii [107] | The Membrane vesicles highly enriched with GS can inhibit the mTOR pathway within macrophages, hindering macrophage migration and M1 polarization. | Intraperitoneal injection | Joint |
| Dexamethasone liposomes [49] | Binding to glucocorticoid receptors on the surface of synovial macrophages promotes their polarization to the M2 phenotype. | Intra-articular injection | Joint |
OA, osteoarthritis; MAGL, Monoacylglycerol lipase; PINK1, Phosphatase and Tensin Homolog-Induced Putative Kinase 1; TGF-β1, transforming growth factor-β1; IL-10, Interleukin-10; PTX-3, Pentraxin-3; IL-4, Interleukin-4; TLR3, Toll-like receptor 3; GS, glutamine synthetase; mTOR, mammalian target of rapamycin.