Résumé
Aim To explore the effeet of soy isofla- vones (SI) on p-amyloid 1 -42 ( Ap, _42 ) -induced hippocampal neuroinflammation and neuronal apoptosis and the underlying mechanism.Methods The prima¬ry hippocampal neurons cultured in vitro were divided into control group (control), Ap,_42 treatment group f model) , SI low-dose group ( Sl-L, 10 mg • L 1 ) , and SI medium-dose group (SI-M, 20 mg • L_l ) and SI high-dose group (SI-H, 40 mg • L 1 ).The model group was treated with 30 (xmol • L"1 Ap, _42 for 48 h; the SI-L, SI-M and SI-H groups were treated with SI for 2 hours, and Ap,_42 was treated for 48 h; the con¬trol group was routinely cultured for 48 h.MTT method was used to detect the survival rate of hippocampal neurons; TUNEL staining was used to detect the apop¬tosis rate of hippocampal neurons; Western blot was used to detect COX-2, TNF-a, NF-kB p65 , P-NF-kB p65, Bcl-2 and caspase-3 protein expression levels.Results Compared with the control group, the surviv¬ al rate of hippocampal neurons was significantly re- duced (P <0.01) , and the apoptotie rate significantly increased (P<0.01).COX-2, TNF-a, p-NF-KB p65 , caspase-3 protein expressions markedly increased (P <0.05 or P <0.01 ) , and the expression of Bcl-2 protein significantly decreased in the model group ( P <0.01 ).Compared with the model group, the surviv¬al rate of hippocampal neurons, Bcl-2 protein in-creased, and the apoptotic rate, the expression of COX-2, TNF-a, p-NF-KB p65 , caspase-3 protein de¬creased (P < 0.05 or P < 0.01 ) in SI each dose group.Conclusion SI can reduce the hippocampal neuroinflammation and neuronal apoptosis induced by APi _42 by inhibiting the activation of NF-kB p65 signa¬ling pathway.