Protective Effects of Exosomes on Osteoarthritis and the Mechanism of Alleviating Cartilage Damage by Regulating PIN1 Expression

Background Osteoarthritis (OA) is a common chronic degenerative joint disease characterized by pathological changes including cartilage degradation, osteophyte formation, and inflammation. Peptidyl-prolyl isomerase 1 (PIN1) regulates cell proliferation, apoptosis, and inflammation, and is implicated in the progression of OA. Exosomes (EXOs), as important mediators of intercellular communication, may protect chondrocytes from inflammatory damage by regulating the PIN1/NF-κB signaling pathway. This study investigated the protective effects and mechanisms of exosomes in alleviating OA cartilage damage by regulating PIN1 expression. Methods EXOs from human umbilical cord mesenchymal stem cells were extracted and characterized by ultracentrifugation. OA model was established in C57BL/6 mice, and exosomes or saline were injected into the joint cavity. Western blot, qRT-PCR, ELISA, and immunohistochemistry were used to examine the expression and distribution of PIN1 and inflammatory factors (IL-6 and TNF-α), and changes in MMP13 and COL2A1 were evaluated. Chondrocytes were cultured in vitro and treated with exosomes, IL-1β, or both. Cell viability and the expression of molecules involved in the PIN1/NF-κB pathway were assessed. Results PIN1 is significantly overexpressed in OA cartilage; exosome treatment significantly downregulated the expression of PIN1 and inflammatory factors, inhibited the upregulation of MMP13, and increased COL2A1 levels. In vitro experiments showed that exosomes attenuated IL-1β-induced PIN1, P65, and MMP13 expression and partially reversed inflammatory damage. Conclusion EXOs can inhibit the PIN1/NF-κB signaling pathway in OA, reduce inflammatory response, and maintain cartilage matrix homeostasis, suggesting that they have potential application value in the treatment of OA.