β-ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration

Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). -ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that -ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that -ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of -ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that -ecdysterone attenuated the apoptosis induced by tert-butyl hydroperoxide via promoting autophagy in nucleus pulposus cells. Beclin-1, an indispensable protein for the stimulation of autophagy, is upregulated and stabilized by -ecdysterone in a dose- and time-dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3-methyladenine partially abrogated the protective function of -ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of -ecdysterone on IDD. Additionally, -ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that -ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that -ecdysterone may be a potential therapeutic agent for IDD.