Icariin induces autophagy and apoptosis of chondrocytes by inhibiting NF-κB signaling pathway
Purpose: To investigate the effect of icariin on autophagy and apoptosis of chondrocytes, and the associated mechanisms.
Methods: The chondrocytes were randomly divided into control (PBS intervention), TNF-α intervention, icarin +TNF-α, and NF-κB inhibition +TNF-α, with 8 strains in each group. The levels of IL-1, IL-6 and IL-12 were assayed by ELISA. The mRNA and protein expressions of ATG5, ATG7, Bax and Bcl-2 cells were determined by polymerase chain reaction (PCR) and Western blotting, while protein expressions of p-p65 and IκBα were assayed using Western blotting.
Results: In the cartilage tissue of rats in the icariin +TNF-α group and NF-κB inhibition +TNF-α group, IL-1, IL-6 and IL-12 levels were significantly lower than those in TNF-α treatment group (p < 0.05). The AATG5 mRNA and protein in cartilage tissues of rats in icariin +TNF-α and NF-κB inhibition +TNF-α groups were significantly higher than those in TNF-α group. Bax mRNA and protein in cartilage tissues of icariin +TNF-α and NF-κB inhibition +TNF-α groups were downregulated, relative to TNF-α group; on the other hand, Bcl-2 mRNA and protein were significantly higher than those of TNF-α group (p < 0.05). In the cartilage tissues of Icarin +TNF-α, NF-κB inhibition +TNF-α groups, P-p65 protein was significantly lower than that of TNF-α (p < 0.05).
Conclusion: TNF-α enhances the production of a large number of inflammatory factors by cartilage cells, inhibits autophagy of cartilage cells, and promotes cell apoptosis through regulation of NF-κB signaling pathway.
Keywords: Icariin, NF-κB signaling pathway, TNF-α, Inflammatory response, Chondrocytes, Autophagy, Apoptosis
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