ArticleInflammopharmacology2023
Adalimumab combined with erythropoietin improves recovery from spinal cord injury by suppressing microglial M1 polarization-mediated neural inflammation and apoptosis.
Article in Inflammopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- An inflammation-targeted lipid nanoparticle inhibiting ferroptosis for spinal cord injury repair.Materials today. Bio · 2026Article
- Effect of adalimumab on anxiety-depression-like behaviors and learning in rats receiving cisplatin.Open medicine (Warsaw, Poland) · 2026Article
- SIK2 mediated mitochondrial homeostasis in spinal cord injury: modulating oxidative stress and the AIM2 inflammasome via CRTC1/CREB signaling.Journal of neuroinflammation · 2025Article
- Muscle Structure and Function Recovery: Adalimumab-Calcium Channel Synergy in Post-Ischemic Stroke Sarcopenia.Journal of cachexia, sarcopenia and muscle · 2025Article
- lncRNA SNHG6 Knockdown Promotes Microglial M2 Polarization and Alleviates Spinal Cord Injury via Regulating the miR-182-5p/NEUROD4 Axis.Applied biochemistry and biotechnology · 2025Article
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
- Regulatory effect of inflammatory mediators in spinal cord injury.Frontiers in immunology · 2025Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAdalimumab (ADM), a humanized antibody against tumour necrosis factor (TNF), is widely applied in treating inflammatory and autoimmune diseases, but its usage in spinal cord injury (SCI) is rarely reported. Hence, this study aimed to explore the effect of ADM with or without erythropoietin (EPO) on microglial polarization, neuroinflammation, neural apoptosis, and functional recovery in SCI.
methodsPrimary microglia were stimulated with lipopolysaccharide (LPS) and then treated with ADM, EPO, or ADM combined with EPO. Then, primary neurons were incubated in the microglial culture medium. SCI rats were established and then treated with ADM, EPO or ADM combined with EPO.
resultsADM suppressed LPS-induced microglial M1 polarization, as reflected by downregulated iNOS and CD86 expression, and neuroinflammation, as reflected by decreased TNF-α, IL-1β, and IL-6 expression, in a dose-dependent manner. Moreover, ADM inhibited microglia-induced neural apoptosis, as reflected by TUNEL assay results and the expression of apoptotic markers (C-Caspase3 and Bcl2), in a dose-dependent manner. EPO monotherapy displayed an effect similar to that of ADM monotherapy. Furthermore, ADM combined with EPO therapy exhibited greater effects than either monotherapy in terms of inhibiting microglial M1 polarization, neuroinflammation, and neural apoptosis. In vivo experiments confirmed the findings of the in vitro experiments and showed that ADM combined with EPO improved SCI functional recovery and neural injury compared with monotherapy.
conclusionADM combined with EPO improves recovery from SCI by suppressing microglial M1 polarization-mediated neural inflammation and apoptosis.
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