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-1β (IL-1β) 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
Method: Human NP cells were isolated and cultured in vitro. NP cells were pretreated with icariin (0.1, 1 and 10
µM) and stimulated by IL-1β (10 ng/ml). The concentration of Prostaglandin E2 was determined by enzymelinked
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, mitogenactivated
protein kinase (MAPK), and nuclear factor-kappa B (NF-κB)-related signaling molecules was assessed
via western blotting.
Results: IL-1β 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-1β-induced production of
degrading enzymes, as well as extracellular matrix reduction. Finally, icariin suppressed IL-1β-induced activation
of MAPK- and NF-κB-related signaling pathways.
Conclusion: The present findings suggest that icariin may have a protective effect on NP cells. The antiinflammatory
effect may contribute to the therapeutic action of icariin in IDD.