Three-N-butyphthalide alleviates early brain injury caused via subarachnoid hemorrhage via activating the LKB-1/ (AMP-activated protein kinase) pathway

Abstract

The influences of 3-N-butyphthalide (NBP) on early brain injury (EBI) induced via mild subarachnoid hemorrhage (SAH) and its mechanism were explored. Establishment of SAH model was via autologous blood injection. The protection of NBP on EBI in SAH model mice was evaluated. Determination of neuronal apoptosis was conducted. Detection of blood brain barrier (BBB), ZO-1, claudin-5, occludin and MMP-9 was manifested. The effects of NBP on oxidative stress, inflammation, and the SIRT1/NF-κB and the LKB-1/AMP-activated protein kinase (AMPK) pathways were investigated. NBP could alleviate neurological deficits and BBB dysfunction, repress cerebral edema and mitigate brain histomorphology. NBP repressed apoptosis in brain tissues, oxidative stress, inflammation, NF-κB activity but facilitated SIRT1. Finally, NBP activated the LKB-1/AMPK pathway. NBP may lighten BBB dysfunction, oxidative stress, inflammation and apoptosis after SAH via activating the LKB-1/AMPK pathway, thereby mitigating EBI.

Keywords:
butyphthalide; LKB-1/AMP-activated protein kinase; subarachnoid hemorrhage; early brain injury