Objective To explore the effect of Anle138b on mitochondrial dysfunction in hippocampal neurons chronicallyex-posed to β-amyloid oligomers(oAβ1-42).Methods We divided mature primary hippocampal neurons fromneonatal Sprague-Dawley rats within 24 h after birth into control group(without any treatment),oAβ1-42 group(treated with 100 nmol/L oAβ1-42 for 7 d),oAβ1-42+Anle138b group(co-treated with 100 nmol/L oAβ1-42 and 100 nmol/L Anle138b for 7 d),and Anle138b group(treated with 100 nmol/L Anle138b for 7 d).After treatment,changes in reactive oxygen species and mitochondrial membrane po-tential(Δφm)-positive cells were measured by flow cytometry.Results According to the factorial analysis of variance,oAβ1-42 and Anle138b had significant main effects(FoAβ1-42=14.149,38.209;FAn1e138b=1.942,24.871;P＜0.01),and there was an interac-tion between oAβ1-42 and Anle138b(Finteraction=18.425,21.904;P＜0.01).The individual effect analysis showed that in the presence of oAβ1-42,Anle138b produced significant effects(F=16.483,19.148;P＜0.01),and in the absence of Anle138b,oAβ1-42 produced significant effects(F=14.149,38.209;P＜0.01).Conclusion Anle138b can reduce oAβ1-42-induced oxidative stress and mito-chondrial damage in hippocampal neurons,inhibiting the damage to hippocampal neurons caused by oAβ1-42.
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