ArticleThe Kaohsiung journal of medical sciences2026
Matrine Attenuates Neurological Deficits and Neuroinflammation by Inhibiting the HMGB1/RAGE Axis and Ferroptosis in Intracerebral Hemorrhage Mice.
Article in The Kaohsiung journal of medical sciences, 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
Intracerebral hemorrhage (ICH) is a life-threatening stroke subtype that lacks effective drug therapy. In the context of ICH, neuroinflammation, and ferroptosis are key contributors to secondary brain injury. In this study, we assessed the neuroprotective effects of matrine (MAT) and its mechanism of action involving the HMGB1/RAGE axis in an ICH mouse model. ICH was induced in mice by autologous blood injection. MAT (1.5 or 20 mg/kg) was administered orally 5 min postinduction. ICH significantly upregulated RAGE and its associated proteins (HMGB1, protein kinase C [PKC], phospholipase C [PLC], and β-amyloid), confirming pathway activation. Molecular docking revealed a specific hydrogen bond interaction between MAT and RAGE but not with PKC or PLC. MAT improved neurological performance, reduced hematoma volume and brain edema, and restored blood-brain barrier integrity through upregulation of tight junction proteins (ZO-1, Occludin, Claudin-4). MAT suppressed activation of the HMGB1/RAGE pathway and downstream kinases JNK, p38, ERK1/2, and NF-κB p65. It also decreased IL-1β, IL-6, and TNF-α levels, reduced Bax, increased Bcl-2, and mitigated neuronal apoptosis. Additionally, MAT lowered Fe
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