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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。
Objective To investigate the effects of astragalosides on the injury of hippocampal neurons induced by dexamethasone (DEX) combined with amyloid β-peptide protein (Aβ) in rats. Methods By examining the activity of hippocampal neurons, we investigated whether Astragalosides can inhibit the decrease of hippocampal neuronal activity induced by Aβ and DEX. Through the determination of intracellular Ca2+ concentration ([Ca2+]i) in hippocampal neurons, we investigated whether Astragalus total glycosides can be decreased [ Ca2+]i inhibited hippocampal neuronal apoptosis; By examining the level of P-tau-Thr231 protein, the mechanism of total hippocampal neuron toxicity induced by Astragaloside Aβ and DEX was further explored. Results Astragalosides (10, 20, 40 μg/mL) had protective effects on fetal rat hippocampal neuronal injury induced by DEX (10 μmol/L) and Aβ25-35 (5 μmol/L) in vitro (P<0.01); The level of [Ca2+]i and P-tau in hippocampal neurons increased significantly by DEX (10 μmol/L) and Aβ25-35 (5 μmol/L) (P<0.05). Conclusion Astragalus has a protective effect on hippocampal neuronal damage induced by Aβ and DEX.