Moracin attenuates LPS-induced inflammation in nucleus pulposus cells via Nrf2/HO-1 and NF-κB/TGF-β pathway
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Updated: Jan 3, 2026

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Published on: January 12, 2020
Ronghe Gu1, Zonggui Huang1, Huijiang Liu1
1Department of Orthopedics, The First People's Hospital of Nanning, Nanning 530022, China.
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.
Insights
Moracin protects intervertebral disc nucleus pulposus cells from inflammation by regulating key cellular pathways. This compound reduces inflammatory cytokines and matrix degradation, offering potential therapeutic benefits.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Intervertebral disc degeneration is linked to inflammation.
- Nucleus pulposus cells are crucial for disc health.
- LPS challenge induces inflammation and matrix degradation in these cells.
Purpose of the Study:
- Investigate moracin's protective effects on nucleus pulposus cells.
- Elucidate the underlying mechanisms of moracin's action.
- Assess moracin's impact on inflammation and matrix degradation.
Main Methods:
- Primary culture of nucleus pulposus cells.
- Lipopolysaccharide (LPS) challenge to induce inflammation.
- Moracin treatment and Nrf-2 knockdown experiments.
- Analysis of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases (MMPs).
- Western blotting and RT-PCR for pathway analysis (Nrf2/HO-1, NF-κB/TGF-β).
Main Results:
- Moracin inhibited LPS-induced inflammatory cytokines (IL-1β, IL-6, TNF-α).
- Moracin reduced oxidative stress markers (MDA) and enhanced antioxidant enzymes (SOD, CAT).
- Moracin reversed LPS-induced changes in Nrf-2, HO-1, NF-κB, IκBα, Smad-3, and TGF-β.
- Moracin decreased matrix degradation enzymes (MMP-3, MMP-13).
- Nrf-2 knockdown abolished moracin's protective effects.
Conclusions:
- Moracin exhibits protective effects against LPS-induced inflammation in nucleus pulposus cells.
- Moracin's mechanism involves regulating the Nrf2/HO-1 and NF-κB/TGF-β pathways.
- Moracin mitigates oxidative stress and matrix degradation, suggesting therapeutic potential for intervertebral disc disorders.
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