Abstract
The present study was designed to investigate the protective effect of moracin on primary culture of nucleus pulposus cells in intervertebral disc and explore the underlying mechanism. Moracin treatment significantly inhibited the LPS-induced inflammatory cytokine accumulation (IL-1β, IL-6 and TNF-α) in nucleus pulposus cells. And moracin also dramatically decreased MDA activity, and increased the levels of SOD and CAT induced by LPS challenge. Moreover, the expressions of Nrf-2 and HO-1 were decreased and the protein levels of p-NF-κBp65, p-IκBα, p-smad-3 and TGF-β were increased by LPS challenge, which were significantly reversed after moracin treatments. Moracin treatments also decreased the levels of matrix degradation enzymes (MMP-3, MMP-13) as indicated by RT-PCR analysis. However, Nrf-2 knockdown abolished these protective effects of moracin. Together, our results demonstrated the ability of moracin to antagonize LPS-mediated inflammation in primary culture of nucleus pulposus in intervertebral disc by partly regulating the Nrf2/HO-1 and NF-κB/TGF-β pathway in nucleus pulposus cells.
Highlights
Growing evidences have shown that the mechanism of pain induced by degeneration of intervertebral disc is still not very clear, and the clinical efficacy is not good
To explore the potential anti-inflammatory effects of moracin, the levels of IL-1β, IL-6 and tissue necrosis factor-α (TNF-α) in the supernatant of primary cell cultures were measured by enzyme-linked immunosorbent assay (ELISA)
As shown in our results, LPS challenge significantly increased the levels of IL-1β, IL-6 and TNF-α in comparison with that in control
Summary
Growing evidences have shown that the mechanism of pain induced by degeneration of intervertebral disc is still not very clear, and the clinical efficacy is not good. Intervertebral disc degeneration, when comes to the condition of cell viability decrease, attenuation of type II collagen and proteoglycan synthesis and dehydration of nucleus pulposus, has been considered as an irreversible process [1]. There is growing evidence that disc degeneration is a disease that is closely related to the nucleus pulposus cells inflammation [3,4]. Inflammation has been suggested to be closely involved in the pathological process of intervertebral disc degeneration [5]. The inflammatory cytokines inducing interleukin-1β (IL-1β), IL-6 and tissue necrosis factor-α (TNF-α) play an important role in intervertebral disc degeneration [6]. Inhibition of the release of inflammatory cytokines is a very effective and feasible solution in preventing degeneration of the intervertebral disc. [7]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
