ArticleMolecular medicine (Cambridge, Mass.)2024
Compound 7 regulates microglia polarization and attenuates radiation-induced myelopathy via the Nrf2 signaling pathway in vivo and in vitro studies.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Insights into the Impact of Low-Dose Ionizing Radiation on Neurodegenerative Disease Progression in In Vivo Models.International journal of molecular sciences · 2026Review
- The mechanism of dynamic switching between M1/M2 phenotypes of microglia in neuropathic pain: a narrative review.Frontiers in molecular neuroscience · 2026Review
- Harnessing Nanocarriers to Improve Psychiatric Treatment: Progress, Limitations, and Future Directions.International journal of nanomedicine · 2026Review
- Identification of a novel and high-affinity cyclic peptide targeting Keap1 for inflammation treatment by a combined virtual screening strategy.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Mechanisms of Keap1/Nrf2 modulation in bacterial infections: implications in persistence and clearance.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundRadiation-induced myelopathy (RM) is a significant complication of radiotherapy with its mechanisms still not fully understood and lacking effective treatments. Compound 7 (C7) is a newly identified, potent, and selective inhibitor of the Keap1-Nrf2 interaction. This study aimed to explore the protective effects and mechanisms of C7 on RM in vitro and in vivo.
methodsWestern blotting, quantitative real-time polymerase chain reaction (qRT-PCR), reactive oxygen species (ROS) and mitochondrial polarization, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, genetic editing techniques, locomotor functions, and tissue staining were employed to explore the protective effects and underlying mechanisms of C7 in radiation-induced primary rat microglia and BV2 cells, as well as RM rat models.
resultsIn this study, we found that C7 inhibited the production of pro-inflammation cytokines and oxidative stress induced by irradiation in vitro. Further, the data revealed that radiation worsened the locomotor functions in rats, and C7 significantly improved histological and functional recovery in RM rats. Mechanically, C7 activated Nrf2 signaling and promoted the microglia transformation from M1 to M2 phenotype.
conclusionC7 could ameliorate RM by boosting Nrf2 signaling and promoting M2 phenotype microglia polarization in vitro and in vivo.
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