Isofraxidin attenuates IL-1β-induced inflammatory response in human nucleus pulposus cells

Inflammation has been demonstrated to be the key factor for intervertebral disc degeneration (IVD), which remains a major public health problem. Isofraxidin is a coumarin compound that possesses strong anti-inflammatory activity. However, the role of isofraxidin in IVD remains unclear. The aim of this study was to evaluate the effects of isofraxidin on inflammatory response in human nucleus pulposus cells (NPCs) exposed to interleukin-1 beta (IL-1 beta). The results proved that isofraxidin attenuated the IL-1 beta-induced significant increases in inflammatory mediators and cytokines including nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha), and IL-6. Besides, isofraxidin also inhibited the induction effect of IL-1 beta on matrix metalloproteinases (MMP)-3 and MMP-13. Moreover, the NF-kappa B activation caused by IL-1 beta was significantly inhibited by isofraxidin treatment. These findings suggested that isofraxidin alleviates IL-1 beta-induced inflammation in NPCs. Our work provided an idea that isofraxidin might act as a novel preventive role in IVD.