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出 处:《中国临床神经外科杂志》2013年第11期681-683,共3页Chinese Journal of Clinical Neurosurgery
摘 要:目的研究刺五加多糖(ASPS)对H2O2诱导的海马神经元凋亡的影响及其机制。方法采用H2O2诱导大鼠海马神经元凋亡。采用末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记法检测细胞凋亡率、免疫组化法检测caspase-3蛋白的表达、逆转录PCR法检测caspase-3 mRNA的表达。结果H2O2作用后,海马神经元凋亡率、caspase-3蛋白和mRNA表达水平均显著增高(P<0.05);给予ASPS干预后,均显著下降(P<0.05);而且,随ASPS剂量增加,作用效果显著增强(P<0.05)。结论ASPS具有抑制氧化应激损伤诱导神经细胞凋亡作用,其机制与下调caspase-3 mRNA的表达有关。ObjectiveTo explore the effect of acanthopanacis senticosi polysaccharides on cell apoptosis induced by H2O2in primary cultured rat hippocampal neurons and its underlying mechanism.MethodsThe cell apoptosis was detected by TUNEL method.The expression level of caspase-3 protein was assessed by positive unit(PU) obtained from immunohistochemical staining imaging. The expression level of caspase-3 mRNA was detected by RT-PCR.ResultsThe rate of cell apoptosis, the expression levels of protein and mRNA of caspase-3 significantly increased in H2O2treated neurons compared with normal neurons. After acanthopanacis senticosi polysaccharides treatment, the rate of cell apoptosis, the expression levels of protein and mRNA of caspase-3 significantly decreased compared with H2O2treated neurons. The protective effect of acanthopanacis senticosi polysaccharides significantly enhanced when the dose increased.ConclusionThe acanthopanacis senticosi polysaccharides has significantly protective effect on cell apoptosis induced by H2O2in primary cultured rat hippocampal neurons and the effect may be attributed to down regulation of caspase-3.
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