Study on the Pharmacological Mechanism of Icariin for the Treatment of Alzheimer's Disease Based on Network Pharmacology and Molecular Docking Techniques

The purpose of this study is to explore the pharmacological mechanism of icariin (ICA) in the treatment of Alzheimer's disease (AD) based on network pharmacology and network molecular docking technology. In order to investigate the regulatory effect of ICA on the expression level of AD pathological phosphorylation regulatory proteins, this study further explored the possible molecular mechanism of ICA regulating AD autophagy through network pharmacology. Macromolecular docking network was verified by Autodock Vina 1.1.2 software. The main active ingredients of ICA, the physicochemical properties, and pharmacokinetic information of ICA were predicted using online databases and relevant information. The results showed that the targets of MAPK3, AKT1, HSP90AA1, ESR1, and HSP90AA1 were more critical in the treatment of AD. Autophagy, apoptosis, senescence factors, phosphatidylinositide 3-kinase/protein kinase B (P13K/AKT) signaling pathway, MAKP, mTOR, and other pathways were significantly associated with AD. Docking of ICA with HIF-1, BNIP3, PINK1, and Parkin pathway molecules showed that the key targets of the signaling pathway were more stably bound to ICA, which may provide a better pathway for ICA to regulate autophagy by providing a better pathway. ICA can improve AD, and its mechanism may be related to the P13K/AKT, MAKP, and mTOR signaling pathways, thereby regulating autophagy-related proteins.