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). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β‑ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β‑ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of β‑ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that β‑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 β‑ecdysterone in a dose‑ and time‑dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3‑methyladenine partially abrogated the protective function of β‑ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β‑ecdysterone on IDD. Additionally, β‑ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β‑ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β‑ecdysterone may be a potential therapeutic agent for IDD.