ArticleImmunity, inflammation and disease2022
Effect of regulating macrophage polarization phenotype on intervertebral disc degeneration.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Tracing the pathways: how inflammatory cytokines and blood metabolites drive intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2025Article
- Pharmacological mechanisms and therapeutic prospects of plant metabolites from traditional Chinese medicine in regulating programmed cell death in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Novel 3-D Macrophage Spheroid Model Reveals Reciprocal Regulation of Immunomechanical Stress and Mechano-Immunological Response.Cellular and molecular bioengineering · 2024Article
- Bioactivities and Mechanisms of Action of Sinomenine and Its Derivatives: A Comprehensive Review.Molecules (Basel, Switzerland) · 2024Review
- Causal relationship of interferon-γ and interleukin-18 upstream of intervertebral disc degeneration pathogenesis: a two-sample Mendelian randomization study.Frontiers in neurology · 2024Article
- Custom-Made Ce-Mn Bimetallic Nanozyme for the Treatment of Intervertebral Disc Degeneration by Inhibiting Oxidative Stress and Modulating Macrophage M1/M2 Polarization.Biomaterials research · 2024Article
- Bioinformatic analysis and identification of macrophage polarization-related genes in intervertebral disc degeneration.American journal of translational research · 2024Article
- The Use of Medical Ozone in Chronic Intervertebral Disc Degeneration Can Be an Etiological and Conservative Treatment.International journal of molecular sciences · 2023Review
- Sinomenine Ameliorates IL-1β-Induced Intervertebral Disc Degeneration in Rats Through Suppressing Inflammation and Oxidative Stress via Keap1/Nrf2/NF-κB Signaling Pathways.Journal of inflammation research · 2023Article
- Immune exposure: how macrophages interact with the nucleus pulposus.Frontiers in immunology · 2023Review
- Effect of regulating macrophage polarization phenotype on intervertebral disc degeneration.Immunity, inflammation and disease · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMacrophages are the only inflammatory cells that can penetrate the closed nucleus pulposus and their polarization plays an important role in intervertebral disc degeneration (IVDD). This paper attempted to investigate the pathogenesis of IVDD by altering the polarization state of macrophages.
methodsMacrophage RAW264.7 cells were induced by interferonγ (IFN-γ) and lipopolysaccharide (LPS). The polarization of RAW264.7 cells was estimated by western blot and immunofluorescence. The expressions of inflammatory factors were detected by ELISA. Subsequently, RAW264.7 cells were treated with different concentrations of minocycline (Mino) and sinomenine (Sino), followed by the assessment of cell viability with cell counting kit-8 kit. Then, RAW264.7 cell culture medium was collected for the culture of human nucleus pulposus cells (NPCs). Toluidine blue staining and type II collagen staining were applied to assay the level of type II collagen. The cell apoptosis, oxidative stress, and nitric oxide (NO) level were appraised by TUNEL, oxidative stress kits and NO kit, respectively. Western blot was employed to test the levels of apoptosis- and oxidative stress-related proteins.
resultsIFN-γ and LPS could induce M1 polarization of RAW264.7 cells. Mino and Sino could reduce the polarization of RAW264.7 cells toward M1. M1-polarized medium inhibited LPS-induced activity, inflammation, and damage of NPCs, which were enhanced by Mino and Sino in medium.
conclusionM1 polarization of macrophages promoted LPS-induced inflammation and damage of NPCs.
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