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PTH Inhibits Senescence in Primary Rat Nucleus Pulposus Cells by Activating Autophagy Induced by Glucocorticoid
Wang Xiaoying, Jiao Liyan, Fu Zhian, He Jinglan*
Department of Orthopedic Surgery, Affiliated Hospital of Hebei University of Engineering, Handan 056002, China
Abstract: Osteoporosis is closely related to the degeneration of the intervertebral disc. Parathyroid hormone (PTH) is thought to relieve the disc degeneration associated with osteoporosis， but its effect on the degeneration of nucleus pulposus cells and disc herniation is not yet clear. In this paper， primary SD rat nucleus pulposus cells were cultured and phenotyped. Nucleus pulposus cells were treated with dexamethasone (DXM) for 48 h. Cell area analysis and β-galactosidase staining were used to analyze the effect of DXM on nucleus pulposus cell senescence. Protein levels of LC3-II， Beclin-1， P62， p-mTOR and p-p70S6k detected by Western blot to analyze the regulatory effect of PTH on the autophagy and mTOR pathway in the cells treated with DXM. After ATG5 siRNA transfection， the regulation of PTH on nucleus pulposus cell senescence and the involvement of autophagy were analyzed. The results showed that as the concentration of DXM increased， the morphology of nucleus pulposus were enlarged and the positive rate of β-galactosidase were increased (P<0.05). PTH increased LC3-II and Beclin-1 protein levels， decreased P62 protein levels and inhibited p-mTOR and p-p70S6k protein expression in DXM-treated nucleus pulposus cells (P<0.05). PTH could attenuate the effect of DXM on the positive rate of β-galactosidase and cellular morphology; However， ATG5 siRNA transfection reversed the protective effect of PTH on cell senescence (P<0.05). The results of this study suggested that PTH might relieve the senescence of nucleus pulposus cells induced by DXM by activating autophagy via mTOR pathway.
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