Acacetin Suppresses IL-1β-Induced Expression of Matrix Metalloproteinases in Chondrocytes and Protects against Osteoarthritis in a Mouse Model by Inhibiting NF-κB Signaling Pathways

Figure 4

Acacetin inhibits IL-1β-induced activation of nuclear factor- (NF-) κB pathways. (a) Chondrocytes were pretreated with acacetin (6.25 μM) for 4 h and then incubated with IL-1β (10 ng/mL) for the indicated time periods (0, 10, and 30 min). The protein levels of p-P38, P38, p-extracellular signal-regulated kinase (ERK), ERK, p-c-Jun N-terminal kinase (JNK), JNK, p-inhibitor of NF-κB-α (IκB-α), and β-actin were determined by western blotting. (b) The quantification of relative protein expression normalized to β-actin. (c) When IL-1β-stimulated chondrocytes were treated with acacetin (6.25 μM), the localization of P65 changed from the nucleus to the cytoplasm. , , and .

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