In the current study, we explored the mechanisms responsible for naringin's protection against TNF-α in an in vitro IDD model and ascertained that naringin-induced autophagic flux increment suppresses inflammation response, oxidative stress, cell apoptosis, and ECM degradation induced by TNF-α via AMPK/SIRT1 activation in human NP cells. The gene discussed is SIRT1; the disease is intervertebral disk degenerative disorder.