Negative effects of high mechanical tensile strain stimulation on chondrocyte injury in vitro.

The mechanism underlying the development of osteoarthritis induced by high tensile strain is unclear. In this study, the effects of different degrees of mechanical tensile strain stimulation on Sprague–Dawley rat chondrocytes were explored. Rat chondrocytes were subjected to mechanical tensile strain at different intensities and frequencies (control group, low tensile strain group, intermediate tensile strain group, and high tensile strain group) using a self-made in vitro tensile strain device. After applying mechanical tensile strain, chondrocytes were collected to detect the expression of collagen II, Aggrecan, matrix metalloproteinase 13 (MMP13), ADAMTS5, and uncoupling protein 2 (UCP2) by real-time quantitative PCR and western blotting as well as reactive oxygen species (ROS) by fluorescence probes. Mechanical tensile strain at different frequencies and intensities had different effects on the biological functions of chondrocytes. Compared with the control group, the expression levels of Col II and Aggrecan in the low and intermediate tensile strain groups increased significantly, while the expression of MMP13 and ADAMTS5 decreased. There were no significant differences between the low and intermediate tensile strain groups. Col II and Aggrecan levels were significantly lower in the high tensile strain group than in the control group, while MMP13 and ADAMTS5 levels were higher. There were no significant differences in ROS production between the low and intermediate tensile strain groups and the control group, but the high tensile strain group exhibited significantly increased ROS production. The expression of UCP2 was significantly lower in the high tensile strain group than in all other groups. These results showed that stimulation with different levels of mechanical tensile strain has different effects on chondrocytes. Repeated high tensile strain promoted the anabolic function of chondrocytes, increased ROS production, and decreased UCP2. These results provide a potential mechanism by which osteoarthritis is induced by high mechanical tensile strain.