ArticleTranslational pediatrics2022
Interleukin-35 exhibits protective effects in a rat model of hypoxic-ischemic encephalopathy through the inhibition of microglia-mediated inflammation.
Article in Translational pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 3 of them syntheses that pooled it.
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Who cites it
7 citing papers in PubMed, 3 syntheses or guidelines pooled it, 10 citations in OpenAlex.
- Hypoxic-Ischemic Encephalopathy: Pathogenesis and Promising Therapies.Molecular neurobiology · 2025Pooled it
- Systematic Review of Interleukin-35 in Endothelial Dysfunction: A New Target for Therapeutic Intervention.Mediators of inflammation · 2025Pooled it
- A systematic review of immune-based interventions for perinatal neuroprotection: closing the gap between animal studies and human trials.Journal of neuroinflammation · 2023Pooled it
- Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Neuroimmune responses in neonatal hypoxic-ischemic encephalopathy: cellular roles, crosstalk, and therapeutic opportunities.Frontiers in pediatrics · 2026Review
- Neuroinflammation and Amyotrophic Lateral Sclerosis: Recent Advances in Anti-Inflammatory Cytokines as Therapeutic Strategies.International journal of molecular sciences · 2025Review
- cGAS Deficiency Regulates the Phenotypic Polarization and Glycolysis of Microglia Through Lactylation in Hypoxic-Ischemic Encephalopathy Cell Model.Biochemical genetics · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hypoxic-ischemic encephalopathy (HIE) brain damage is related to inflammatory responses and oxidative stress. Interleukin (IL)-35 is an antioxidant and anti-inflammatory cytokine. Thus, the effect of IL-35 treatment on neonatal rats with hypoxic-ischemic brain injury was investigated. Methods: A total of 96 7-day-old Sprague Dawley rats were randomly divided into three groups: sham group, HIE group, and IL-35 group. After left common carotid occlusion and 2.5 h hypoxia (HI injury), IL-35 (20 µg/g) was intraperitoneally (i.p.) administered to the pups. Results: Administration of IL-35 alleviated neurological deficiencies, decreased brain edema, ameliorated cerebral infarction, and limited M1 microglial polarization in HI-injured pups. Meanwhile, IL-35 decreased pro-inflammatory cytokines, tumor necrosis factor-α, IL-1β, and reactive oxygen species generation in OGD-induced bEnd.3 cells. Furthermore, IL-35 treatment could reverse the vascular endothelial cell injury induced by microglial polarization. Finally, IL-35 markedly suppressed the activation of hypoxia-inducible factor-1α (HIF-1α) and the nuclear factor-κB (NF-κB) signaling pathway Conclusions: IL-35 relieved hypoxic-ischemic-induced brain injury and inhibited the inflammatory response by suppressing microglial polarization and activation. These results suggest that IL-35 might have potential applications for the treatment of HIE.
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