ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026
Berberine targets the PI3Kα LYS672 site to suppress the PI3K/Akt/NF-κB axis and modulate microglial functional states after intracerebral hemorrhage.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 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
Microglia-driven neuroinflammation contributes to secondary injury after intracerebral hemorrhage (ICH). Modulating microglial functional states represents a promising therapeutic strategy. Berberine (BBR) has neuroprotective effects, but its role in ICH remains unclear. This study investigated whether BBR alleviates ICH-induced neuroinflammation by modulating microglial responses after ICH via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor kappa-B (NF-κB) axis. Network pharmacology predicted BBR targets. An ICH mouse model was used to assess BBR's effects on hematoma volume, neurological function and neuroinflammation. Transcriptomics identified differentially expressed genes and enriched pathways. Immunofluorescence assessed glial activation, cell death and extracellular matrix remodeling. In lipopolysaccharide-stimulated BV2 cell, microglial functional states and PI3K/Akt/NF-κB signaling were evaluated by Western blotting and immunofluorescence, with the mechanism clarified via molecular docking, inhibitors, and an activator. Network pharmacology identified 208 common targets enriched in inflammatory and extracellular matrix pathways. In vivo, BBR reduced hematoma volume, improved neurological outcomes, attenuated neuronal damage, and suppressed glial activation and cell death. Transcriptomics revealed BBR reversed ICH-induced inflammatory and extracellular matrix-related gene expression. In vitro, BBR shifted microglia from pro-inflammatory to anti-inflammatory phenotype and rebalanced cytokine expression. Molecular docking identified PI3K as a primary target, and Western blotting confirmed BBR suppressed PI3K/Akt/NF-κB signaling, validated by inhibitors. Notably, the PI3K agonist failed to reverse BBR's inhibition, reinforcing PI3K as a key functional target. BBR targets the PI3Kα LYS672 site to inhibit downstream NF-κB, thereby regulating microglial functional states and alleviating post-ICH neuroinflammation. These findings support BBR as a potential ICH therapeutic.
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