Icariin Induces Chondrocyte Degeneration via Activation of the <scp>NF</scp>‐<scp>κB</scp> Signalling Pathway and Reduces the Inflammation Factor Expression Induced by Lipopolysaccharide

To investigate the effect of icariin on chondrocytes by activating the nuclear factor kappa-B (NF-κB) signalling pathway and the mechanism of icariin in inducing chondrocytes degeneration. Chondrocytes were cultured in vitro and treated with icariin at concentrations of 0, 0.01, 0.1, 10 and 20 μm. Cell proliferation was evaluated by cell counting kit-8 (CCK8) method, apoptosis was detected by TUNEL method and the expression of NF-κB was detected by Western blotting (WB) and RT-PCR. The nuclear localization of NF-κB p65 protein was observed by immunofluorescence staining. Lipopolysaccharide (LPS) was used to establish the inflammatory model, and WB and RT-PCR were used to detect the expression levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). After treatment with icariin, the proliferation ability of chondrocytes was markedly enhanced, and the apoptosis rate (AR) was markedly decreased (p < 0.05). In addition, icariin could inhibit the nuclear translocation of NF-κB p65 protein, promote the gene expression of Collagen II (Col-II) and Aggrecan in chondrocytes, and reduce the expression of NF-κB. Moreover, icariin markedly reduced the expression of IL-6 and TNF-α in LPS-induced inflammation (p < 0.05). Icariin can enhance chondrocyte proliferation, promote phenotypic gene expression by inhibiting the NF-κB signal transduction pathways, thus suppressing the chondrocyte degeneration, and can reduce the inflammation factor expression induced by LPS.