ArticleCNS neuroscience & therapeutics2025
AD16 Modulates Microglial Activation and Polarization to Mitigate Neuroinflammation in Ischemic Stroke Models Through α7nAChR-ERK-STAT3 Signaling.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The Protective Mechanism of Continuous Theta Burst Stimulation in the Acute Phase of Stroke Through Modulation of the Calcineurin/AKT/FOXO1 Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- IncRNAs transcriptomics elucidates the potential mechanism of Naoshuantong capsule in alleviating synaptic dysfunction in a murine model of cerebral ischemia/reperfusion injury.Frontiers in pharmacology · 2026Article
- AD16 Modulates Microglial Activation and Polarization to Mitigate Neuroinflammation in Ischemic Stroke Models Through α7nAChR-ERK-STAT3 Signaling.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundNeuroinflammation constitutes a critical pathological event subsequent to ischemic stroke. AD16, a novel anti-neuroinflammatory compound, has demonstrated efficacy in alleviating neuroinflammation in neonatal rats induced by ischemia-hypoxia. This study aims to elucidate the therapeutic utility and underlying mechanisms of AD16 in an adult ischemic stroke rat model.
methodsA rat transient middle cerebral artery occlusion (tMCAO) model was employed. Neurological function was evaluated using the Longa and Garcia JH scores, motor function was assessed through rotary rod and CatWalk gait analysis, and brain injury was examined via TTC and Nissl staining. Molecular docking techniques simulate the binding of a target compound to a potential target. Western blot, immunofluorescence, and enzyme-linked immunosorbent assay (ELISA) were used to detect microglia phenotype, pro-inflammatory factors, and activation of signaling molecules.
resultsAD16 treatment improved neural function in tMCAO rats, reduced cerebral infarction volume and brain water content, preserved blood-brain barrier integrity, and inhibited pro-inflammatory cytokines. Molecular docking showed AD16 has high affinity for α7nAChR, TLR4, ERK, and STAT3. AD16 increased α7nAChR, CD206, and p-ERK protein levels, while decreasing CD40, CD68, TLR4, and p-STAT3. These effects were reversed by α-BTX (α7nAChR inhibitor) and U0126 (ERK inhibitor).
conclusionAD16 may inhibit microglia activation and polarization via the α7nAChR-ERK-STAT3 pathway, thus reducing neuroinflammation from cerebral ischemia and protecting the brain. This study suggests AD16 as a potential treatment for ischemic stroke.
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