To determine the efficacy and specific mechanism of vitamin D on intervertebral disc degeneration. The model of intervertebral disc degeneration was established in 3-month-old mice. Furthermore, the levels of intervertebral disc degeneration in the vitamin D group and the control group were detected one month later by X-ray, Western boltting, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) et al. In addition, in vitro, we cultured mouse intervertebral disc nucleus pulposus cells to verify the effect of vitamin D on nucleus pulposus cells and study its mechanism. In vivo, compared with the control group, mice in the vitamin D group showed dose-dependent retardation of intervertebral disc degeneration in terms of reducing inflammatory responses, antioxidant stress, inhibiting apoptosis and delaying cell aging. In vitro, compared with the control group, collagen II was increased and collagen X was decreased in mice treated with vitamin D. In vivo and in vitro experiments, the expression of p65 and IκB kinase α was decreased and the expression of inhibitor of NF-κB was increased in the intervertebral disc tissue or nucleus pulposus cells of the vitamin D treatment group, indicating that vitamin D could suppress the NF-κB pathway. Vitamin D retarded intervertebral disc degeneration by inhibiting NF-κB pathway, which may relieve inflammatory reactions, resist oxidative stress, inhibit apoptosis and delay cell senescence.
Keywords: Intervertebral disc degeneration; NF-κB pathway; vitamin D.