Erk activation and proliferation in osteoarthritc chondrocytes after continuous passive motion
10.3969/j.issn.2095-4344.2016.42.005
- VernacularTitle:持续被动运动条件下骨关节炎软骨细胞Erk活性及增殖
- Author:
Yi HU
;
Yunping REN
;
Yong ZHANG
;
Daohai XIONG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2016;20(42):6265-6270
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Whether continuous passive motion improves osteoarthritis by enhancing the proliferation ability of chondrocytes is rarely reported.
OBJECTIVE:To analyze the therapeutic outcomes of continuous passive motion in rabbits with osteoarthritis and the underlying mechanism.
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.
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.
