Analysing the anti-AD effect of Fuzi and its potential molecular mechanism.
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.
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.
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.