Abstract
Intervertebral disc degeneration (IDD) is a natural progression of the aging process associated with inflammation. Higenamine, a plant-based alkaloid, has been identified to possess various pharmacological properties, including anti-inflammatory activity. In the present study, we aimed to evaluate the role of higenamine in interleukin (IL)-1β-induced inflammation in human nucleus pulposus cells (NPCs). The results showed that higenamine improved cell viability in IL-1β-induced NPCs. The IL-1β-dependent up-regulation of inflammatory molecules including inducible nitric oxide synthase (iNOS), nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), and IL-6 was attenuated by higenamine in NPCs. The increased productions of matrix metalloproteinases (MMP-3 and MMP-13), as well as a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS-4 and ADAMTS-5) were significantly mitigated by higenamine treatment. Furthermore, we also found that higenamine suppressed the IL-1β-induced activation of NF-κB signaling pathway in NPCs. In conclusion, the present study proved that higenamine exhibited anti-inflammatory activity against IL-1β-induced inflammation in NPCs via inhibiting NF-κB signaling pathway. These results suggested that higenamine might be a therapeutic agent for the treatment of IDD.
Highlights
Intervertebral disc degeneration (IDD) is a natural progression of the aging process that common causes lower back pain, representing a serious socio-economic burden [1]
Higenamine improved cell viability in nucleus pulposus cell (NPC) exposed to IL-1β
Higenamine decreases the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in IL-1β-stimulated NPCs
Summary
Intervertebral disc degeneration (IDD) is a natural progression of the aging process that common causes lower back pain, representing a serious socio-economic burden [1]. It is evident that IDD is closely associated with inflammatory response, which is mediated by the abnormal production of pro-inflammatory molecules secreted by both the nucleus pulposus (NP) and the annulus fibrosus (AF) [2]. An elevation in levels of inflammatory cytokines is observed. Some cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1 α/β, IL-6, and IL-17 can promote matrix degradation, chemokine production, and results in changes in cell phenotype, thereby initiating a cascade of degenerative events [3,4]. In addition to the role in the onset of the inflammatory condition, a number of proinflammatory mediators play crucial role in the development of IDD [3]. Inhibition of the production of cytokines may be new approach for treating IDD
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