Erk activation and proliferation in osteoarthritc chondrocytes after continuous passive motion

Muyesaier?Maimaitiniyazi; Hu Yi; Ren Yun-ping; Zhang Yong; Xiong Dao-hai

doi:10.3969/j.issn.2095-4344.2016.42.005

Abstract：BACKGROUND:Whether continuous passive motion improves osteoarthritis by enhancing the proliferation ability of chondrocytes is rarely reported. <br> OBJECTIVE:To analyze the therapeutic outcomes of continuous passive motion in rabbits with osteoarthritis and the underlying mechanism. <br> METHODS:Thirty-six New Zealand white rabbits were randomly al otted into three groups (n=12 per group). Rabbits in control group only underwent capsulotomy with no harm to the cartilage;osteoarthritis models were established in the rabbits of model and treatment groups using Hulth method. At 1 day after modeling, the treatment group rabbits were treated with continuous passive motion, 8 hours daily for consecutive 8 weeks. Interleukin-1 and tumor necrosis factorαlevels in the synovial fluid were detected by ELISA;col agen type II expression and the proliferation ability of chondrocytes were detected by MTT assay;Erk signaling pathway activation was determined using western blot assay. <br> RESULTS AND CONCLUSION:In the model group, interleukin-1 and tumor necrosis factorαlevels in the synovial fluid were significantly increased, and the expression level of col agen type II mRNA was remarkablely down-regulated. Continuous passive motion significantly downregulated interleukin-1 and tumor necrosis factorαlevels and up-regulated the col agen type II mRNA level (P<0.01). The model group showed significantly decreased proliferation ability of chondrocytes and down-regulated Erk signaling pathway activation, while after continuous passive motion, al above indicators were significantly improved (P<0.01). These results indicate that the continuous passive motion can al eviate osteoarthritis probably by influencing interleukin-1 and tumor necrosis factorαlevels, proliferation ability of chondrocytes, and col agen type II expression, as wel as regulating Erk signaling pathway activation.