alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis.

is a herbal medicine used to treat osteoarthritis (OA) in Chinese traditional medicine. However, the molecular mechanisms underlying the therapeutic effects of this medicinal herb against OA have rarely been reported. Given that it has been established that extracellular matrix metabolism plays an important role in the pathogenesis of OA, the present study focused on the effects and mechanisms of in the regulation of extracellular matrix metabolism in chondrocytes induced by IL-1β. Rat chondrocytes were isolated, cultured and identified . The CCK-8 method was used to detect the cell viability of aqueous extract (BCAE)-treated chondrocytes. The chondrocyte inflammatory and degeneration models were induced by 10 ng/mL IL-1β, then chondrocytes were grouped into different groups to evaluate the effect of BCAE on extracellular matrix degradation and the regulation of TLR4/NF-κB signaling pathway. Furthermore, whether the regulatory effect of BCAE on TLR4/NF-κB signaling pathway is related to miRNA-145-5p was also investigated by cell transfection. We found that BCAE promoted chondrocyte viability in a dose- and time-dependent manner. BCAE delayed chondrocyte degeneration induced by IL-1β. BCAE could reduce the degradation of the cartilage extracellular matrix by inhibiting the TLR4/NF-κB signaling pathway. miRNA-145-5p negatively regulated the expression of TLR4 in chondrocytes, while BCAE could upregulate the expression of miRNA-145-5p in chondrocytes induced by IL-1β. These results suggest that BCAE upregulates the expression of miRNA-145-5p to inhibit the TLR4/NF-κB signaling pathway, thereby alleviating the metabolic imbalance of the extracellular matrix and protecting chondrocytes from degeneration.