Effect of β-asarone on ischemic brain injury in rats

AimTo investigate the therapeutic effects of β-asarone, a key active component of Acorus tatarinowii, on rats with ischemic stroke.MethodsMiddle cerebral artery occlusion (MCAO) rats were established by using the intraluminal filament method and divided into the sham, model, β-asarone (various doses), and positive drug control groups. Treatments were administered for 7 d. The neurological deficit scores, Nissl staining for Nissl body morphology and density, NeuN protein, inflammatory cytokines were assessed. Network pharmacology was used to identify potential targets. To validate epidermal growth factor receptor (EGFR) involvement, the EGFR inhibitor was intracerebroventricularly injected 30 min before MCAO induction, followed by β-asarone treatment for 7 d. An in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in PC12 cells. After β-asarone intervention, the cell viability, NeuN, EGFR protein levels, and inflammatory cytokines were measured by CCK-8 assay, Western blot and RT-qPCR, respectively. EGFR inhibitor was used to confirm pathway specificity.Resultsβ-asarone significantly improved neurological function in MCAO rats, increased Nissl body density and NeuN protein levels, and suppressed IL-1β, TNF-α, and IL-6 expression. In vitro, β-asarone protected PC12 cells against OGD/R-induced damage. Network pharmacology identified 121 potential targets for β-asarone in ischemic stroke, with enrichment analysis linking its mechanism to the EGFR signaling pathway. Western blot confirmed β-asarone upregulated EGFR. EGFR inhibition abolished β-asarone's neuroprotective effects.Conclusionβ-asarone exerts protective effects against ischemic stroke by activating the EGFR signaling pathway.