Fig. 5
The therapeutic efficacy of representative anti-senescence drugs with different mechanisms of action in vitro and in vivo. a Gastrodin regulates phosphorylation of the PI3K-AKT pathway via SIRT3, reduces SA-β-gal positive staining in IL-1β-treated chondrocytes, and reverses cartilage destruction in the OA rat model.226 Permission of reuse obatained from copyright holder Elsevier. b Chondrocyte cultures supplemented with exosomes from umbilical cord MSCs significantly reduce SA-β-gal positive staining of OA chondrocytes and improve articular cartilage bulk structure.213 Permission of reuse obtained from copy right holder American Chemical Society. c Cerium dioxide nanoparticles reduce the percentage of SA-β-gal-positive cells in H2O2-treated synoviocytes and protect articular cartilage by scavenging ROS and inactivating the NF-κB signaling pathway.207 Permission of reuse obtained from copyright holder MDPI. d Multi-kinase inhibitor YKL-05-099 inhibit MAPK and NF-κB signaling activation by affecting kinome phosphorylation, reduce IL-1β-induced chondrocyte senescence, decrease the level of senescence markers p21Clp1 and p16INK4A in chondrocytes, and prevent subchondral bone loss effectively.212 Permission of reuse obtained from copyright holder The Author(s). e Small copper sulfide nanoparticles functionalized with anti-beta-2-microglobulin antibodies specifically induce apoptosis in senescent chondrocytes and prevent articular cartilage damage.233 Permission of reuse obtained from copyright holder The Author(s). f Rapamycin decreases the levels of senescence markers in H2O2-stimulated human chondrocytes and reduces joint P16INK4a positivity in the mouse OA model by upregulating autophagy.210 Permission of reuse obtained from copyright holder The Author(s)
