Protective effects of psoralidin on IL‑1β‑induced chondrocyte apoptosis

Chondrocyte apoptosis serves a key role in the pathogenesis of osteoarthritis. The present study aimed to investigate the protective effects of psoralidin on interleukin (IL)‑1β‑induced chondrocyte apoptosis and explore the underlying mechanisms. Chondrocytes were isolated from the articular cartilage of Sprague‑Dawley rats and were treated with 10 ng/ml IL‑1β and various doses of psoralidin (5, 10 or 15 µM). The ratio of apoptosis was measured by Annexin V/propidium iodide double‑labeling fluorescence‑activated cell sorting (FACS) analysis. Caspase‑3 and ‑9 activity was determined using a quantitative colorimetric assay. Intracellular levels of reactive oxygen species (ROS) were assessed using a dichlorofluorescein diacetate‑labeling FACS analysis, and the release of nitric oxide (NO) was measured using the Griess reaction method. In addition, protein expression levels were detected by western blotting. The results of the present study demonstrated that psoralidin may reduce IL‑1β‑induced chondrocyte apoptosis. Psoralidin pretreatment also reversed the inhibitory effects of IL‑1β on B‑cell lymphoma 2 (Bcl‑2) expression, and decreased the IL‑1β‑induced expression of Bcl‑2‑associated X protein, matrix metalloproteinase (MMP)‑1 and MMP‑13. Furthermore, psoralidin decreased IL‑1β‑induced caspase‑3 and ‑9 activity, NO release, ROS production and nuclear factor (NF)‑κB nuclear translocation. In addition, the NF‑κB inhibitor pyrriolidine‑dithiocarbamate exerted similar effects to psoralidin, thus suggesting that IL‑1β induced proapoptotic effects in rat chondrocytes via an NF‑κB‑dependent pathway. Since psoralidin could protect chondrocytes from IL‑1β‑induced apoptosis and MMP expression, the present results suggested that psoralidin may be considered a drug candidate for the treatment of osteoarthritis.