Effects of Roubin-manipulation on apoptosis of chondrocytes and expression of Bcl-2, Bax and Fas in rabbit knee joint

BACKGROUND: Modern studies have demonstrated that excessive cellular apoptosis accelerates the degeneration of cartilaginous tissue. However, effects of mechanical stimulation of manipulation on joint cartilage at the molecular level have been rarely reported. OBJECTIVE: To observe the effects of Roubin-mamipulation on apoptosis of chondrocytes and expression of Bcl-2, Bax and Fas in rabbit knee joint. METHODS: Fifty New Zealand rabbits were randomly divided into normal, sham operation, model, manipulation, and sodium hyaluronate groups. Rabbits in the latter three groups were established into high intraosseous pressure experiment model of right leg by ligating the vena femoralis and gluteae inferiors. One week later, the manipulation group received 10-minute Roubin-manipulation, once every other day, a total of 17 times within 5 weeks. The sodium hyaluronate group received intra-articular injection of 0.6 mL sodium hyaluronate, once a week, for a total of 5 times. RESULTS AND CONCLUSION: At the end of the 8 th week, cartilaginous tissue of medial tibial plateau of rabbit right knee joint was harvested. Hematoxylin-eosin staining showed that compared with normal group, cartilaginous tissue degeneration was obvious, and chondrocyte apoptosis rate was significantly increased (P < 0.01), and Bcl-2, Bax and Fas expression in the tibial cartilaginous tissue was significantly increased (P < 0.01) in the model group. Compared with the model group, the cartilaginous tissue degeneration was slight, chondrocyte apoptosis rate and Bax and Fas expression were significantly decreased (P < 0.01), but Bcl-2 expression in the tibial cartilaginous tissue was significantly increased (P < 0.01) in the manipulation and sodium hyaluronate groups. Roubin-mamipulation, like intra-articular injection of sodium hyaluronate, can obviously decrease the apoptosis rate of chondrocytes in rabbit knee joint and the underlying mechanisms are related to upregulated Bcl-2 expression and downregulated Bax and Fas expression.