Objective: To investigate the neuroprotective effects and mechanism of luteolin against β-amyloid 25-35(Aβ25-35) induced neural damage. Method: Primary neurons were isolated and purified from cerebral cortex of suckling mouse of BALB/c. The experiment was assigned three groups. The control group

the model group (neurons were co-cultured with Aβ25-35 incubation for 12 h and luteolin administration (neurons were co-cultured with Aβ25-35 and luteolin incubation for 12 h). water soluble tetrazolium sait(WST-1) method was used to test cell viability. The apoptosis was examined by Hoechst 33258/propidum iodide(PI) double staining. The expression of Caspase-3 was analyzed by the Western bolt; reactive oxygen species(ROS) was examined by 2'

7'-dichlorofluorescin diacetate(DCFH-DA) assay. The productions of tumor necrosis factor-α(TNF-α) and interleukin-10(IL-10) were measured using enzyme-linked immunosorbant assay (ELISA) kits. Result: WST-1 assay results displayed that the cellular viability of model group was 48.5% and had significant differences compared to control group. Cellular viability of Aβ25-35-induced cells exposed to 10

30

60

90 μmol·L-1 of luteolin was 60.8%

62.4%

71.7%

73.6% and then 60 μmol·L-1 of luteolin was choose for the next experiments. 60 μmol·L-1 of luteolin obviously increased cell viability to 71.7%;Hoechst 33258 nuclear staining and PI double staining showed that luteolin could significantly decrease apoptotic rate compared with the Aβ25-35 treated group;luteolin inhibited Caspase-3 and ROS of neurons induced by Aβ25-35. Compared with model group

luteolin also decreased the productions of TNF-α to 176.7 ng·L-1 and increased IL-10 to 634.8 ng·L-1(P <0.05). Conclusion: Luteolin possesses the neuroprotective effects on Aβ25-35 damaged neurons

which may be associated with inhibition of ROS

up-regulation of anti-inflammatory cytokine IL-10

down-regulating of Caspase-3 and TNF-α to against neurons apoptosis.