ArticleCell communication and signaling : CCS2026
Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundStatus epilepticus (SE) is a life-threatening neurological emergency with high mortality, often leading to acute cerebral edema and chronic cognitive impairment. Its pathology involves both immune and vascular dysfunction. The complement C3/C3a receptor (C3/C3aR) signaling pathway has recently emerged as a key regulator of immune activation and blood-brain barrier (BBB) permeability. This study investigates whether bindarit, a potent anti-inflammatory drug, mitigates SE-induced brain injury through modulation of the C3/C3aR pathway.
methodsSE modeling mice were randomized to receive daily bindarit or vehicle. To explore underlying mechanisms, C3aR antagonist (C3aRA) and recombinant C3a were used in additional groups. Post-SE brain injuries were assessed, including survival, memory performance, histopathology, brain edema, BBB integrity, neurovascular inflammation, microglia-astrocyte interactions, and microglial synaptic engulfment.
resultsWe found that bindarit treatment improved survival and memory, reduced histological damage, alleviated brain edema, preserved BBB integrity, and attenuated endothelial inflammation in SE mice. It promoted a shift in microglia from a pro-inflammatory to an anti-inflammatory-associated features, reversed pathological microglia-astrocyte crosstalk, limited synaptic elimination, and restored microglial morphology. Mechanistically, bindarit inhibited neurotoxic astrocyte-derived C3 production and reduced C3aR expression in both microglia and endothelial cells. C3aRA produced comparable protective effects, whereas co-administration of C3a partially negated bindarit’s benefits.
conclusionsBindarit confers robust neuroprotection in SE by preserving BBB integrity, attenuating neurovascular inflammation, reducing synaptic loss, and improving cognitive outcomes. These effects are mediated predominantly through inhibition of the C3/C3aR pathway, highlighting bindarit as a promising therapeutic candidate for SE.
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