Objective: To investigate the neuroprotective effects and mechanism of taxifolin against Aβ induced neural damage. Method: Primary neurons were isolated and purified from cerebral cortex of suckling mouse. The neurons were co-cultured with Aβ and taxifolin for 24 h. CCK8 method was used to test cell viability. The apoptosis was examined by Hoechst 33258 nuclear staining

Annexin V-FITC/PI double staining and caspase-3 activity. Result: In cell viability

compared with the normal group

cell viability of model group decreased significantly (49.2±1.3) %

different concentrations of taxifolin could improve the neuronal activity

the cell viability of 80 μmol·L-1 taxifolin increased to (68.7±3.2)%

compared with the model group. Compared with the normal group

the apoptosis rate of model group was (50.8±1.5)% (P<0.01)

different concentrations of taxifolin could reduce the cell apoptosis rate

40 μmol·L-1 taxifolin apoptosis rate was (41.5±2.7)%

compared with the model group (P<0.05). Compared with the normal group

in model group

caspase-3 activity was (2.37±0.16) U·μg-1(P<0.01)

compared with the model group

40 μmol·L-1 taxifolin group decreased the caspase-3 activity (1.77±0.07) U·μg-1(P<0.01). CCK8 assay displayed that taxifolin obviously increased cell viability. Hoechst 33258 nuclear staining and Annexin V-FITC/PI double staining showed that taxifolin could significantly decrease apoptotic rate compared with the Aβ treated group. Taxifolin also inhibited caspase-3 activity of neurons induced by Aβ. Conclusion: Taxifolin possesses the neuroprotective effects on Aβ damaged neurons

which may be associated with inhibition of caspase-3 activity in neurons to against apoptosis.