知母皂苷BⅡ对Aβ_(25-35)诱导的原代大鼠神经细胞损伤的保护作用

目的研究甾体皂苷类化合物知母皂苷BⅡ对Aβ25-35诱导的原代大鼠神经细胞损伤的保护作用。方法体外培养原代大鼠神经细胞,采用MTT(四甲基偶氮唑盐)法检测细胞增殖活性;采用分光光度法测定细胞培养液中LDH(乳酸脱氢酶)漏出率、SOD(超氧化物歧化酶)活力、MDA(丙二醛)含量以及AChE(乙酰胆碱酯酶)活力。结果知母皂苷BⅡ10-4、10-5mol.L-1能明显增强Aβ25-35(20μmol.L-1)诱导的神经细胞增殖活性,降低LDH漏出率,并能明显提高其SOD活力、降低MDA含量,同时对AChE活力具有一定的降低作用。结论知母皂苷BⅡ能明显改善Aβ25-35诱导的原代大鼠神经细胞损伤,可能与其提高模型细胞的抗氧化能力,改善胆碱能系统相关。

Protective effects of timosaponin BⅡ on primary neurons against beta amyloid peptide 25-35

Aim To study the protective effects of timosaponin BⅡ on primary neurons against beta amyloid peptide 25-35 induced toxicity.Methods Immunofluorescence was used to identify primary neurons.MTT(tetrazolium salt) assay was used to measure neurons metabolic state.Spectrophotometric method was used to measure the release of LDH(lactate dehydrogenase),the activity of SOD(superoxide dismutase),the activity of AChE(acetylcholine) and the production of MDA(malonaldehyde) in the culture medium.Results Treatment with beta amyloid peptide 25-35(20 μmol·L-1) for 24 h caused a significant damage in primary neurons.Timosaponin BⅡ 10-4、10-5 mol·L-1 markedly improved neurons metabolic activity,decresed the release of LDH and the production of MDA,markedly increased the activity of SOD and decresed the activity of AChE.Conclusion Timosaponin BⅡ could significantly reduce the neurotoxicity induced by beta amyloid peptide 25-35 in primary neurons.The mechanism of which may be related with resisting oxidative damage and regulating the cholinergic system.