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Coenzyme Q10 (Co-Q10) is extraordinarily popular and has been used in abundant interventions as an antioxidant reagent that participates in numerous oxidation reactions. According to substantial evidence previously reported, interleukin-1β (IL-1β) is deemed to be one of the chief orchestrator molecules in the degeneration of intervertebral disc (IVD). However, it is unknown whether Co-Q10 is able to protect against IVD degeneration. In the current study, mouse-derived IVDs as well as primary human nucleus pulposus (NP) cells were isolated and cultured. NP cells were stimulated with IL-1β, with or without selective addition of Co-Q10 to investigate the therapeutic effect of Co-Q10 on IVD degeneration. Levels of IL-1β-induced inflammatory biomarkers including TNF-α, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-κB signaling activation. Furthermore, Co-Q10 maintained the production of anabolic biomarkers in NP cells such as collagen 2, aggrecan and Sox-9 and altered the enhanced catabolism induced by IL-1β. Moreover, the therapeutic role of Co-Q10 in sustaining IVD tissue-enhanced anabolism is potentially dependent on activation of the Akt signaling pathway. In summary, Co-Q10 may potentially represent an available molecular target that may shed light on approaches to the prevention and treatment of IVD degeneration in the future.Co-Q10 inhibits IL-1β induced catabolism in NP cells.Co-Q10 promotes anabolism in NP cells.Co-Q10 protects against IVD degeneration via NF-κB and Akt signaling pathways.