【摘要】 目的:探索淫羊藿素(icaritin,ICT)对Aβ25-35肽致大鼠原代培养神经细胞的损伤保护作用及潜在机制。方法:制备d17胎龄大鼠胚胎皮层神经细胞,支持培养7d后,与ICT预孵育24h并加入Aβ25-35肽,作用72h后以细胞形态、MTT值、培养液乳酸脱氢酶(LDH)水平作为细胞的损伤指标;并以线粒体膜电位(ΔΨm)改变作为凋亡早期指标,AO/EB染色差异作为凋亡后期指标。结果:0.1μmol·L-1ICT预孵育24h能显著改善10μmol·L-1Aβ25-35肽所致的原代培养神经细胞的损伤,MTT、LDH及形态学结果显示:ICT能提高Aβ25-35肽损伤神经细胞的存活率,JC-1染色结果显示:ICT能防止Aβ25-35肽诱导的细胞线粒体ΔΨm下降,AO/EB染色结果显示:ICT能够改善神经细胞凋亡。结论:ICT经抗凋亡机制对Aβ25-35肽损伤大鼠原代培养神经细胞发挥保护作用。该作用与ICT干预Aβ25-35肽诱导的细胞线粒体膜电位下降和核损伤有关。更多还原

【Abstract】 Objective: To investigate the protective effects of icaritin (ICT) on apoptosis of primarily cultured rat neurons induced by Aβ25-35 peptide and its mechanism. Methods: Cortical neurons from rat embryonic cortical on d17 pregnancy were cultured in neural basal medium for 7 days.Icaritin (ICT) was pre-incubated for 24 h before adding Aβ25-35 peptide and then the cells were incubated for 72h.Neuroprotective effects of ICT were evaluated by MTT assay,LDH level in medium and cell morphological observation.Meanwhile,apoptosis was determined by JC-1 staining for mitochondria membrane potential (ΔΨm) and AO/EB double staining for genetic damage of nucleoli in monolayer cells. Results: 0.1 μmol·L-1ICT pre-incubation for 24 h prevented rat neurons from Aβ25-35 peptide induced apoptosis significantly as demonstrated by MTT,LDH assay and morphological observation.AO/EB double staining also indicated that ICT prevented neurons from apoptosis.JC-1 staining further showed that ICT prevented decreasing of mitochondrial ΔΨm induced by Aβ25-35 peptide. Conclusion: ICT could protect primarily cultured rat neurons from Aβ25-35 peptide induced apoptosis.更多还原