Dioscin Attenuates Interleukin 1β (IL-1β)-Induced Catabolism and Apoptosis via Modulating the Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling in Human Nucleus Pulposus Cells.

Abstract

BackgroundNucleus pulposus (NP) cell dysfunction and apoptosis contribute to disc degeneration. Dioscin, a natural steroid saponin, has been demonstrated to have anti-inflammatory, antiapoptotic, and antioxidative effects in various diseases. However, little is known about the roles of dioscin in intervertebral disc degeneration.Material/MethodsTo evaluate the roles of dioscin in disc degeneration and its specific mechanism, human NP cells were incubated with IL-1β and various concentrations of dioscin. Cell viability, extracellular matrix protein expression, catabolic factors, degree of apoptosis, inflammatory factors, and related signaling pathways were evaluated by western blotting, fluorescence immunostaining, TUNEL staining, and reverse transcription PCR.ResultsDioscin inhibited IL-1β-activated apoptotic signaling and catabolic activity in NP cells. Dioscin suppressed TLR4/NF-0κB signaling, and attenuated the level of inflammatory mediators (IL-6, TNF-α) in IL-1β-stimulated human NP cells.ConclusionsOur work provides the first evidence that dioscin attenuates IL-1β-activated inflammation and catabolic activity in human NP cells through inhibiting the TLR4/NF-κB pathway, indicating that dioscin is a new potential candidate for clinical therapy to attenuate disc degeneration.