inhibits Alzheimer's disease by regulating the complex regulation network with the core of and .

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.