Abstract

Biatractylolide is an Atractylodes macrocephala derived bisesquiterpenoid that has been found treatment of dementia in model mice. This study aims to explore the therapeutic effect on vascular dementia. Network pharmacological techniques have been used to elaborate the involved mechanisms of biatractylolide treating vascular dementia. Based on PubChem database, Swiss target prediction and human gene database GeneCards, 19 common target molecules were screened, they were enriched in many biological, such as Alzheimer’s disease corrective pathway, pathways of neurodegeneration-multiple diseases, calcium signaling pathway, notch signaling pathway and vascular endothelial growth factor signaling pathway. Muscarinic acetylcholine receptor M1, amyloid-beta precursor protein, microtubule-associated protein tau, presenilin-1, presenilin-2, prostaglandin G/H synthase 2 and disintegrin, and metalloproteinase domain-containing protein 17 were enriched in Alzheimer’s disease corrective pathway. Protein–protein interaction network presents that six highest degree nodes, phosphoinositide-3-kinase regulatory subunit 1, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, Harvey rat sarcoma virus, Jun N-terminal kinases, catenin beta 1, mitogen-activated protein kinase 3 and tumor protein P53, play core role in vascular dementia and four molecules, mitogen-activated protein kinase 14, Janus kinase 2, amyloid-beta precursor protein and tyrosine-protein phosphatase non-receptor type 1, closely interact with biatractylolide. In addition, acetylcholinesterase was identified to have a strong interaction with biatractylolide. This study suggests that biatractylolide is a potential drug for treatment of vascular dementia or Alzheimer’s disease.