Anisodine hydrobromide injection promotes neural remodeling and recovery after ischemic stroke in mice.

Abstract

Anisodine hydrobromide injection has shown promising therapeutic effects in treating patients with cerebral infarction, improving recovery of neurological function during the post-cerebral infarction period. However, the effects of anisodine hydrobromide on brain recovery and neuroplasticity are unclear. This study explores the therapeutic effects and underlying mechanisms of anisodine hydrobromide in mice experiencing the chronic phase of an ischemia stroke. The electrocautery method established a distal middle cerebral artery occlusion (MCAO) model in healthy male C57BL/6 mice. Neurological deficits were evaluated using Golgi and immunofluorescence staining to measure the effects of anisodine hydrobromide on neural proliferation, migration and remodeling. DAPT (dipeptidic γ-secretase-specific inhibitor) was employed to explore the involvement of the Notch signaling pathway post-anisodine hydrobromide treatment. Compared to the control and MCAO groups, mice treated with anisodine hydrobromide showed improved post-stroke neurological function, increased neurite intersections, and dendritic spine density in the peri-infarct cortex. Anisodine hydrobromide also promoted neural cell regeneration which is dendritic and axonal structures and synaptic vesicle protein restructuring. Gap43, NGF, Notch1, and Hes1 protein level increased significantly in the ANI group provided inhibitor DAPT was absent. Anisodine hydrobromide can promote neurological function, neurotrophic factors, and neuroplasticity. Notch signaling pathways also impact the effects of anisodine hydrobromide on neural plasticity in ischemia stroke.