Inhibits Alzheimer's Disease by Regulating the Complex Regulation Network with the Core of and
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Context: Current medicine for Alzheimer's disease (AD) cannot effectively reverse or block nerve injury. Traditional Chinese Medicine practice and research imply (Fuzi) may meet this goal.
Objective: Analysing the anti-AD effect of Fuzi and its potential molecular mechanism.
Materials And Methods: AD model cells were treated with Fuzi in 0-300 mg/mL for 24 h in 37 °C. The cell viability (CV) and length of cell projections (LCP) for each group were observed, analysed, and standardised using control as a baseline (CV and LCP). The Fuzi and AD relevant genes were identified basing on databases, and the molecular mechanism of Fuzi anti-AD was predicted by network analysis.
Results: Experiment results showed that Fuzi in 0.4 mg/mL boosted LCP (LCP = 1.2533, ≤ 0.05), and in 1.6-100 mg/mL increased CV (CV from 1.1673 to 1.3321, ≤ 0.05). Bioinformatics analysis found 17 Fuzi target genes (relevant scores ≥ 20), showing strong AD relevant signals (RMS_ ≤ 0.05, related scores ≥ 5), enriched in the pathways regulating axon growth, synaptic plasticity, cell survival, proliferation, apoptosis, and death ( ≤ 0.05). Especially, and interacted with protein and located in the key point of the "Alzheimer's disease" pathway.
Discussion And Conclusions: These results suggest that Fuzi may have therapeutic and prevention potential in AD, and and may be the core of the pathways of the Fuzi anti-AD process. Fuzi should be studied more extensively, especially for the prevention of AD.
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