ArticleMolecular neurobiology2025
The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Gut-brain-immune interactions in neonatal hypoxic-ischemic brain injury.Molecular and cellular pediatrics · 2026Review
- CaMKIIα inhibition facilitates functional recovery after preterm hypoxic-ischemic brain injury by disrupting microglial GPNMB signaling.Translational pediatrics · 2026Article
- Article
- Heat stress induced testicular impairment is related to orchitis and complement activation in Rongchang boars.Journal of animal science and biotechnology · 2025Article
- Butyrate-Mediated Upregulation of Insulin Pathway Gene Expression Suggests Potential Antidiabetic Effects.Drug development research · 2025Article
- Epigenetic Dysregulation in Neurodegenerative Disease: Implications for Neuropathology and Therapy.Cureus · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perinatal asphyxia is one of the most important causes of morbidity and mortality in newborns. One of the key pathogenic factors in hypoxic-ischemic (HI) brain injury is the inflammatory reaction including complement system activation. Over-activated complement stimulates cells to release inflammatory molecules and is involved in the post-ischemic degradation of synaptic connections. On the other hand, complement is also involved in regenerative processes. The histone deacetylase inhibitor (HDACi)-sodium butyrate (SB)-provides reduction of inflammation by decreasing the expression of the proinflammatory factors. The main purpose of this study was to examine the effect of SB treatment on complement activation and synapse elimination after HI. Neonatal HI was induced in Wistar rats pups by unilateral ligation of the common carotid artery followed by 60-min hypoxia (7.6% O2). SB (300 mg/kg) was administered on a 5-day regimen. Our study has shown decreased levels of synapsin I, synaptophysin, and PSD-95 in the hypoxic-ischemic hemisphere, indicating synaptic loss after neonatal HI. Transmission electron microscopy revealed injury of the synaptic structures in the brain after HI. SB treatment increased the level of the synaptic proteins, improved tissue ultrastructure, and reduced degradation of the synapses. Neonatal HI induced mRNA expression of the complement C1q, C3, C5, and C9, and their receptors C3aR and C5aR. The effect of SB was different depending on the time after induction of hypoxic-ischemic damage. Our study demonstrated that neuroprotective effect of SB may be related to the modulation of complement activity after HI brain injury.
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