Pharmaceutical Biology · 2022 · 19 citations · 32 references
MedicineNeurosciencePharmacologyCell SignalingMolecular NeuroscienceMolecular PharmacologyNeurodegeneration MechanismsNeurodegenerative Disease PharmacologyNeurodegenerative DiseasesNeurodegenerative DisordersNeuroprotectionNeuroprotective PharmacologyAlzheimer Disease NeuroprotectionNeuroactive CompoundsNeuroprotective AgentsNeuroprotective MechanismsNeuroprotective SignalingPharmacological Treatment Of DementiaProtein Interaction Network TopologyProtein-protein Interaction Network Analysis
CONTEXT: Ursolic acid (UA) and acteoside (ATS) are important active components that have been used to treat Alzheimer's disease (AD) because of their neuroprotective effects, but the exact mechanism is still unclear. OBJECTIVE: Network pharmacology was used to explore the mechanism of UA + ATS in treating AD, and cell experiments were used to verify the mechanism. MATERIALS AND METHODS: + solvent pre-treatment), UA (5 μM), ATS (40 μM), UA (5 μM) + ATS (40 μM). Then apoptosis, mitochondrial membrane potential, caspase-3 activity, ATG5, Beclin-1 protein expression and Akt, mTOR phosphorylation levels were detected. RESULTS: : 250 μM) nerve damage by enhancing cells viability, combating apoptosis, restoring MMP, reducing the activation of caspase-3, lessening the phosphorylation of Akt and mTOR, and increasing the expression of ATG5 and Beclin-1. CONCLUSIONS: -induced neurotrosis by regulation of AKT/mTOR signalling.
32
Loss of autophagy in the central nervous system causes neurodegeneration in mice
Masaaki Komatsu, Satoshi Waguri, Tomoki Chiba et al. · Nature · 2006 · 3.5K citations
GeneCards Version 3: the human gene integrator
Marilyn Safran, Irina Dalah, Jake M. Alexander et al. · Database · 2010 · 2.1K citations · Full text