Breviscapine

Breviscapine (Breviscapinun) is a flavonoid compound with antioxidant, anti-inflammatory, anti-fibrotic, and neuroprotective activities. Breviscapine ameliorates cerebral ischemia/reperfusion injury and vascular dementia, and inhibits the formation of postoperative abdominal adhesions. The mechanism of action of Breviscapine involves the regulation of oxidative stress, inflammatory cytokines, signaling pathways such as TGF-β/Smad, and cellular calcium overload. Breviscapine is used for research on diseases including cardiovascular and cerebrovascular diseases^[1][2][3]. In Vitro:Breviscapine (6.25-100 μg/L; 24 h) protects primary cortical neurons against H₂O₂-induced cytotoxicity and increases cell viability to 76.51 ^[1].
Breviscapine (50 μg/L; 24 h) reduces H₂O₂-induced intracellular calcium overload in primary cortical neurons^[1]. In Vivo:Breviscapine (2 mg/kg; i.p.; 14 days) significantly improves learning and memory function, restores antioxidant balance, and alleviates neuronal histopathological damage in rats with vascular dementia induced by permanent bilateral common carotid artery ligation^[1].
Breviscapine (10-40 mg/kg; i.p.; 10 days) significantly inhibits the formation of postoperative intra-abdominal adhesions in Wistar rats by suppressing inflammatory responses, upregulating peritoneal fibrinolytic activity, and regulating the TGF-β/Smad signaling pathway^[2].
Breviscapine (20-100 mg/kg; i.p.; administration starts 7 days before MCAO and continues until sacrifice) dose-dependently alleviates cerebral ischemia/reperfusion injury in Sprague-Dawley rats. Among all regimens, the 100 mg/kg daily i.p. dose initiated 7 days prior to surgery exerts the optimal efficacy, including reducing cerebral infarct volume by approximately 55%, and significantly improving neurological function, levels of inflammatory markers, oxidative stress status, and apoptotic signaling pathways^[3].