Anti-Alzheimer’s Disease Molecular Mechanism of Acori Tatarinowii Rhizoma Based on Network Pharmacology

Abstract

Background:Acori Tatarinowii Rhizoma (ATR), a traditional Chinese herbal medicine, is used to treat Alzheimer's disease (AD), which is a worldwide degenerative brain disease. The aim of this study was to identify the potential mechanism and molecular targets of ATR in AD by using network pharmacology. Material/Methods:The potential targets of the active ingredients of ATR were predicted by PharmMapper, and the targets of Alzheimer's disease were searched by DisGeNET. All screened genes were intersected to obtain potential targets for the active ingredients of ATR. The protein-protein interaction network of possible targets was established by STRING, GO Enrichment, and KEGG pathway enrichment analyses using the Annotation of DAVID database. Next, Cytoscape was used to build the "components-targets-pathways" networks. Additionally, a "disease-component-gene-pathways" network was constructed and verified by molecular docking methods. In addition, the active constituents b-asarone and b-caryophyllene were used to detect Ab 1-42 -mediated SH-SY5Y cells, and mRNA expression levels of APP, Tau, and core target genes were estimated by qRT-PCR. Results:The results showed that the active components of ATR participate in related biological processes such as cancer, inflammation, cellular metabolism, and metabolic pathways and are closely related to the 13 predictive targets: ESR1, PPARG, AR, CASP3, JAK2, MAPK14, MAP2K1, ABL1, PTPN1, NR3C1, MET, INSR, and PRKACA. The ATR active components of b-caryophyllene significantly reduced the mRNA expression levels of APP, TAU, ESR1, PTPN1, and JAK2. Conclusions:The targets and mechanism corresponding to the active ingredients of ATR were investigated systematically, and novel ideas and directions were provided to further study the mechanism of ATR in AD.

Multi-Target Effects of ß-Caryophyllene and Carnosic Acid at the Crossroads of Mitochondrial Dysfunction and Neurodegeneration: From Oxidative Stress to Microglia-Mediated Neuroinflammation

“…It also ameliorated Aβ1–42-induced neuro-inflammation in BV-2 microglial cells through the suppression of TLR4, NO, PGE2, iNOS, and COX-2 expression, and the secretion of pro-inflammatory cytokines [ 96 ]. Recently, Zhang and colleagues [ 280 ] have shown that BCP may protect SH-SY5Y cells against Aβ neurotoxicity via the inhibition of JAK2 expression. BACE1 protein is crucial for the synthesis of amyloid precursor protein (APP).…”

Effects of Moleac 901 after severe spinal cord injury on chronic phase in Wistar rats

“…SCI-induced secondary damage leads to further neuronal cell loss by apoptosis cell death mediated by intracellular caspase proteases [ 8 ]. Activating the caspase-3 proenzyme triggers the death of nerve cells in SCI during the chronic phase [ 4 , 9 ].…”