Objective To determine the effect of aspirin on the expression of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), nuclear factor-kappa B (NF-κB)/p65 and total protein phosphorylated inhibitor protein α of nuclear factor κB (pIκB-α) in neuroinflammation induced by β amyloid protein 25-35 (Aβ25-35) in order to investigate the role of NF-κB pathway in this process. Methods Hippocampal neurons were freshly isolated from fetal SD rats at embryonic day 17 to 18 and cultured for 7d. Then the neurons were randomly divided into 4 groups, that is, Aβ treatment group (20 μmol/L Aβ25-35), low dose aspirin group (50 μmol/L aspirin and 20μmol/L Aβ25-35), high dose aspirin group (100μmol/L aspirin and 20μmol/L Aβ25-35), and the blank control group. After 48 hours’ treatment, the levels of IL-1β and TNF-α in the supernatant were measured with ELISA, and the expression level of NF-κB/p65 and pIκB-α with Western blotting. Results Compared with the control group, Aβ treatment remarkably resulted in higher levels of TNF-α and IL-1β (P＜0.01), as well as the expression of NF-κB/p65 and pIκB-α (P＜0.01). Compared with Aβ group, low dose and high dose aspirin groups had lower levels of TNF-α and IL-1β (P＜0.05), as well as the expression of NF-κB/p65 and pIκB-α (P＜0.05). There were no statistical differences between the low and high aspirin groups (P＞0.05). Conclusion Aspirin attenuates neuronal inflammatory injury induced by Aβ25-35 through inhibiting the activation of NF-κB.