ArticleBioscience reports2019
Moracin attenuates LPS-induced inflammation in nucleus pulposus cells via Nrf2/HO-1 and NF-κB/TGF-β pathway.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Superoxide dismutase in intervertebral disc degeneration: from pathophysiological mechanism to therapeutic strategies.Molecular biology reports · 2026Review
- Hierarchical assembly of traditional chinese medicine-based hydrogels for wound healing.Journal of nanobiotechnology · 2026Review
- Therapeutic targeting of Nrf2/HO-1/NF-κB signaling axis with casticin mitigates intervertebral disc degeneration: in vitro and in vivo investigations.In vitro cellular & developmental biology. Animal · 2025Article
- Serum antioxidant enzymes in spinal stenosis patients with lumbar disc herniation: correlation with degeneration severity and spinal fusion rate.BMC musculoskeletal disorders · 2023Article
- The Pivotal Role of Nrf2 Signal Axis in Intervertebral Disc Degeneration.Journal of inflammation research · 2023Review
- Suppressive Effect of Tetrahydrocurcumin onOxidative medicine and cellular longevity · 2022Article
- Mitochondrial quality control in intervertebral disc degeneration.Experimental & molecular medicine · 2021Review
- Pharmacological Targeting of Heme Oxygenase-1 in Osteoarthritis.Antioxidants (Basel, Switzerland) · 2021Review
- Bardoxolone Methyl Ameliorates Compression-Induced Oxidative Stress Damage of Nucleus Pulposus Cells and Intervertebral Disc DegenerationFrontiers in bioengineering and biotechnology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.