Background: Explore the mechanism of "miR-27b-3p targeting BDNF inhibits the TrkB/CREB signaling pathway and improves IL-1 β-induced chondrocyte inflammation".Methods: The animal and cell models of arthritis were constructed, and various biochemical detection methods were used to detect the changes of apoptosis, inflammation and oxidative stress.Results: The results showed that the expression of miR-27b-3p was downregulated in IL-1β-treated chondrocytes and cartilage tissues isolated from a KOA rat model. miR-27b-3p overexpression notably reduced IL-1β-induced chondrocyte apoptosis and the expression levels of caspase-3 and caspase-9. In addition, cell transfection with miR-27b-3p mimics increased the mRNA and protein expression levels of inducible nitric oxide synthase and cyclooxygenase-2. The levels of nitric oxide, prostaglandin E2 (PGE2), TNF-α and IL-6 were also reduced following cell transfection with miR-27b-3p mimics. Furthermore, bioinformatics analysis predicted that miR-27b-3p could directly target brain-derived neurotrophic factor (BDNF). Additionally, the present study suggested that the tropomyosin receptor kinase B (TrkB)/cAMP response‑element binding protein (CREB) signaling axis could be a downstream pathway of the miR-27b-3p/BDNF axis. The percentage of apoptotic cells and the expression levels of nitric oxide, PGE2, TNF-α and IL-6 were enhanced in chondrocytes co-treated with BDNF + IL-1β. However, these effects were restored following transfection of chondrocytes with miR-27b-3p mimics. Staining of cartilage tissues with safranin O showed that miR-27b-3p overexpression Significantly attenuated KOA-induced cartilage degradation.Conclusions:miR-27b-3p targeting BDNF inhibits the TrkB/CREB signaling pathway and improves IL-1 β-induced chondrocyte inflammation.