[关键词]
[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。
[Key word]
[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(P0.01).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)(P0.05).Conclusion AST could protect hippocampal neuron against synergistic neurotoxicity of Aβ and DEX.
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[基金项目]
安徽省高校省学术带头人科学研究资助项目(2005hbz18);安徽省教育厅高等学校优秀青年人才基金资助项目(2009SQRZ050)