ArticleCell death discovery2020
Parthenolide promotes the repair of spinal cord injury by modulating M1/M2 polarization via the NF-κB and STAT 1/3 signaling pathway.
Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.
- Advances in the research of the role of macrophage/microglia polarization-mediated inflammatory response in spinal cord injury.Frontiers in immunology · 2022Pooled it
- The SHEDs-derived apoptotic bodies for inflammatory regulation in spinal cord repair.NPJ Regenerative medicine · 2026Article
- Sappanone A Promotes Motor Function Recovery in Spinal Cord Injury Mice by Inhibiting Microglial M1 Polarization via Activation of the Keap1/Nrf2 Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Electroacupuncture at Huatuo-Jiaji acupoints combined with conductive hydrogel synergistically improves bladder and motor functions after spinal cord injury.Materials today. Bio · 2025Article
- The neuroinflammatory triumvirate: NF-κB, NLRP3, and mTOR in spinal cord injury.Inflammopharmacology · 2025Review
- Investigating the Effects of Epac2 Activation in an In Vitro Cortical Mechanical Injury Model for Central Nervous System Repair.The European journal of neuroscience · 2025Article
- Targeting JAK/STAT signaling pathway by curcumin: implications for spinal cord injury neuroprotection.Inflammopharmacology · 2025Review
- Silencing of SH3BP2 Inhibits Microglia Activation Via the JAK/STAT Signaling in Spinal Cord Injury Models.Inflammation · 2025Article
- Article
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- NF-κB inhibition attenuates sympathetic hyperreflexia and concomitant development of autonomic dysreflexia and immune dysfunction after spinal cord injury.Communications biology · 2025Article
- Human dental pulp stem cells for spinal cord injury.Stem cell research & therapy · 2025Review
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries.Cureus · 2025Review
- SIX1 aggravates the progression of spinal cord injury in mice by promoting M1 polarization of microglia.Scientific reports · 2025Article
- Article
- Macrophage Polarization in the Osteoarthritis Pathogenesis and Treatment.Orthopaedic surgery · 2025Review
- Dolutegravir Derivatives Alleviate LPS-Induced Microglial Inflammation by Suppressing STAT1/3 Nuclear Translocation.Drug design, development and therapy · 2025Article
- Parthenolide ameliorates 3-nitropropionic acid-induced Huntington's disease-like aberrations via modulating NLRP3 inflammasome, reducing microglial activation and inducing astrocyte shifting.Molecular medicine (Cambridge, Mass.) · 2024Article
- Sonic Hedgehog reduces inflammatory response, decreases blood-spinal cord barrier permeability, and improves locomotor function recovery in an acute spinal cord injury rat model.Journal of inflammation (London, England) · 2024Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a severe neurological disease; however, there is no effective treatment for spinal cord injury. Neuroinflammation involves the activation of resident microglia and the infiltration of macrophages is the major pathogenesis of SCI secondary injury and considered to be the therapeutic target of SCI. Parthenolide (PN) has been reported to exert anti-inflammatory effects in fever, migraines, arthritis, and superficial inflammation; however, the role of PN in SCI therapeutics has not been clarified. In this study, we showed that PN could improve the functional recovery of spinal cord in mice as revealed by increased BMS scores and decreased cavity of spinal cord injury in vivo. Immunofluorescence staining experiments confirmed that PN could promote axonal regeneration, increase myelin reconstitution, reduce chondroitin sulfate formation, inhibit scar hyperplasia, suppress the activation of A1 neurotoxic reactive astrocytes and facilitate shift from M1 to M2 polarization of microglia/macrophages. To verify how PN exerts its effects on microglia/macrophages polarization, we performed the mechanism study in vitro in microglia cell line BV-2. PN could significantly reduce M1 polarization in BV2 cells and partially rescue the decrease in the expression of M2 phenotype markers of microglia/macrophage induced by LPS, but no significant effect on M2 polarization stimulated with IL-4 was observed. Further study demonstrated PN inhibited NF-κB signal pathway directly or indirectly, and suppressed activation of signal transducer and activator of transcription 1 or 3 (STAT1/3) via reducing the expression of HDAC1 and subsequently increasing the levels of STAT1/3 acetylation. Overall, our study illustrated that PN may be a promising strategy for traumatic SCI.
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