The molecular mechanism of treating osteoarthritis with dipsacus saponins by inhibiting chondrocyte apoptosis

Abstract

The present study aimed to determine the molecular mechanism of treating osteoarthritis with dipsacus saponins by inhibiting the apoptosis of chondrocytes. A total of 30 New Zealand rabbits were randomly divided into 2 groups: A control group and a model group. The osteoarthritis model was established using the HULTH method. The success of the model establishment was determined by pathological morphology and measurement of inflammatory cytokine levels. Chondrocytes were isolated and divided into 4 groups treated with varying concentrations of dipsacus saponins: 0, 25, 50 and l00 μg/l dipsacus saponins. Cell cycle distribu­tion was analyzed using flow cytometry. Changes in cyclin D1, cyclin‑dependent kinase 4 (CDK4) and p21 expression were detected by western blotting and changes in the levels of Bcl‑2, Bax, caspase‑3 and caspase‑9 mRNA were detected using reverse transcription‑quantitative polymerase chain reaction. The osteoarthritis model was established success­fully, indicated by a significant increase in the levels of IL‑1β, IL‑6 and TNF‑α in the model group (P<0.05) compared with the control group. The viability of the chondrocytes increased following treatment with dipsacus saponins in a concentra­tion‑dependent manner. The number of chondrocytes in the G0/G1 phase decreased in the 50 and l00 μg/l groups while the number of chondrocytes in the G2/M phase increased in the 50 and l00 μg/l groups. Levels of cyclin D1 and CDK4 expres­sion increased following treatment with dipsacus saponins. Levels of Bax, caspase‑3 and caspase‑9 expression decreased while Bcl‑2 levels increased following treatment with dipsacus saponins. The viability of chondrocytes increased following treatment with dipsacus saponins in a concentration‑dependent manner. Thus, dipsacus saponins inhibited the apoptosis of chondrocytes by up‑regulating Bcl‑2 and down‑regulating caspase‑9, caspase‑3 and Bax expression.