【摘要】 目的探讨黄芪总苷(astragalosides)对地塞米松(Dexamethasone,DEX)与β-淀粉样蛋白(Amyloidβ-peptide protein,Aβ)联合诱导大鼠海马神经元损伤的影响。方法通过检测海马神经元细胞活性,探讨黄芪总苷能否抑制Aβ和DEX引起海马神经元活力下降;通过检测海马神经元胞内Ca2+浓度([Ca2+]i),探讨黄芪总苷是否通过降低[Ca2+]i抑制海马神经元凋亡;通过检测P-tau-Thr231蛋白水平,进一步探讨黄芪总苷抗Aβ和DEX引起的海马神经元毒性机制。结果 黄芪总苷(10、20、40μg/mL)对体外DEX(10μmo/L)+Aβ25-35(5μmol/L)引起胎鼠海马神经元的损伤有保护作用(P<0.01);黄芪总苷能明显降低DEX(10μmol/L)+Aβ25-35(5μmol/L)升高的海马神经元[Ca2+]i、P-tau蛋白水平(P<0.05)。结论黄芪总苷对Aβ和DEX诱导的大鼠海马神经元损伤有一定的保护作用。更多还原

【Abstract】 Objective To study the effect of astragaloside(AST) on the injury induced by amyloid β-protein(Aβ) plus Dexamethasone(DEX) in rat hippocampal neurons.Methods In vitro,the effects of AST on hippocampal neurons cell death with Aβ plus DEX were detected by MTT assay and intracellular calcium(i);The effects of AST on phospho-tau(P-tau) protein were analyzed to explore the mechanisms responsible for DEX enhanced Aβ-induced cell death in hippocampal neurons.Results AST(10,20,and 40 μg/mL) could protect hippocampal neurons against DEX(10 μmol/L) plus Aβ25-35(5 μmol/L)-induced hippocampal neuronal injury of felal rat in vitro(P<0.01).AST could inhibit the increased levels of i and P-tau protein level induced by DEX(10 μmol/L) plus Aβ25-35(5 μmol/L)(P<0.05).Conclusion AST could protect hippocampal neuron against synergistic neurotoxicity of Aβ and DEX.更多还原