Icariin Attenuates Interleukin-1β-Induced Inflammatory Response in Human Nucleus Pulposus Cells

Background: Low back pain is a common problem, mainly caused by intervertebral disc degeneration (IDD). An important pathophysiological characteristic of IDD is the loss of homeostatic balance of the extracellular matrix metabolism. Interleukin-1 beta (IL-1 beta) is one of the inflammatory mediators stimulating the degradation of extracellular matrix in the nucleus pulposus (NP) and contributing to IDD pathogenesis. Icariin, which is isolated from Epimedium brevicornum, acts as an anti-inflammatory drug. Objective: This study aimed to explore the pharmacological effects of icariin in IDD by simulating NP inflammation in vitro. Method: Human NP cells were isolated and cultured in vitro. NP cells were pretreated with icariin (0.1, 1 and 10 mu M) and stimulated by IL-1 beta (10 ng/ml). The concentration of Prostaglandin E2 was determined by enzyme-linked immunosorbent assay. Nitric oxide was determined by Griess reagent assay. The expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), degrading enzymes, collagen II, aggrecan, mitogen-activated protein kinase (MAPK), and nuclear factor-kappa B (NF-kappa B)-related signaling molecules was assessed via western blotting. Results: IL-1 beta induced pronounced expression of COX-2 and iNOS, and stimulated production of prostaglandin E2 and nitric oxide. Icariin exhibited significant anti-inflammatory effect, inhibiting IL-1 beta-induced production of degrading enzymes, as well as extracellular matrix reduction. Finally, icariin suppressed IL-1 beta-induced activation of MAPK-and NF-kappa B-related signaling pathways. Conclusion: The present findings suggest that icariin may have a protective effect on NP cells. The anti-inflammatory effect may contribute to the therapeutic action of icariin in IDD.