Effect of Calcitonin on the Inflammatory Reaction in IL-1β-induced Chondrocytes in Rats

Objective To investigate the effects of calcitonin( CT) on the expressions of matrix metalloproteinase-13( MMP-13),type Ⅱ collagen( Col Ⅱ),p38 and P-p38 in interleukin-1β( IL-1β) induced osteoarthritis( OA)rats. Methods Sprague-Dawley rats' chondrocytes were isolated and cultured. The chondrocytes were identified by Toluidin Blue staining. The second-generation chondrocytes were divided into control group with complete medium,IL-1β-induced group with 10 ng / ml IL-1β of complete medium and CT treatment group with 50 ng / ml CT after being added with the 10 ng / ml IL-1β of complete medium for 15 min,and the three groups were all cultured for 24 h. The ultrastructural changes were observed under transmission electron microscope,and the expressions of MMP-13,ColⅡ,P38 and p-P38 were detected using Western-blot method,and realtime quantified polymerase chain reaction( PCR) was used to detect MMP-13 and ColⅡ mRNA expressions. Results There were no significant differences in p38 protein and mRNA expressions of chondrocytes in the three groups( P 0. 05). The expressions of p-P38,MMP-13 and mRNA in IL-1β-induced and CT treatment groups were significantly higher than those in control group,but the expressions in CT treatment group was lower than those in IL-1β-induced group( P 0. 05); the expressions of ColⅡ and mRNA in IL-1β-induced and CT treatment groups were significantly lower than those in control group( P 0. 05),and the expressions in CT treatment group were higher than those in IL-1β-induced group,but the differences were not statistically significant( P 0. 05).Conclusion IL-1β may induce OA pathological change of rats' chondrocytes in vitro. Calcitonin may improve IL-1β induced chondrocytes injury in OA rat models to a certain degree,and one of the mechanisms may inhibit the activation of the P38 signaling pathway to reduce the MMP-13 expression,and therefore the degradation of Col Ⅱ will be reduced and the OA process will be delayed.