灵芝多糖对β淀粉样蛋白诱导大鼠海马神经元细胞损伤的保护作用  

Protective Effects of Ganoderan on Apoptosis of Cultured Hippocampus Neurons Induced by Aβ_(1-40)

作　　者：谈震[1] 范守文[2] 

机构地区：[1]江苏省省级机关医院,江苏南京210024 [2]南京中医药大学,江苏南京210029

出　　处：《药物生物技术》2010年第5期430-433,共4页Pharmaceutical Biotechnology

摘　　要：研究灵芝多糖对β淀粉样蛋白1-40(Aβ1-40)诱导体外培养大鼠海马神经元凋亡的保护作用以及可能的作用机制。体外培养新生Wistar大鼠海马神经元,MTT法检测不同浓度灵芝多糖干预Aβ1-40的细胞毒作用,选择出现显著拮抗细胞毒性的剂量为使用剂量。用HO33342检测细胞凋亡情况,用RT-PCR技术检测凋亡相关基因bcl-2、bax和caspase3基因mRNA的表达水平。结果显示10μmol/L Aβ1-40与海马神经元共孵育48h有明显的细胞毒作用,并可诱导神经元凋亡,加入不同浓度灵芝多糖后凋亡细胞明显不同程度减少。Aβ1-40可使bcl-2基因表达下调,bax基因表达上调,caspase-3基因的表达增强。加入灵芝多糖干预后,部分拮抗了Aβ1-40诱导的bcl-2基因的表达变化,从而使caspase-3基因的表达降低。灵芝多糖可通过调控bcl-2/bax的比值,降低caspase-3基因mRNA的表达来阻断Aβ1-40所诱导的海马神经元凋亡,具有神经保护作用。To study the protective effects of ganoderan on apoptosis of cultured hippocampus neurons induced by Aβ1-40,and to explore the possible mechanism,neurotoxicity was measured by MTT assay among the cultured hippocampus neurons treated with Aβ1-40 and different concentrations of ganoderan.The concentration which ganoderan protected the neurons from injuring by Aβ1-40,was determined.Apoptosis was manifested by HO33342 staining,and the expression levels of bcl-2,bax and caspase-3 were analyzed by RT-PCR.Results showed that significant neurotoxicity of neurons was observed after incubating with 10μmol/L Aβ1-40 for 48h.Excessive apoptosis was observed among the neurons under the same condition,such as down regulation of bcl-2 expression and up regulation of bax expression.The apoptotic index（bcl-2/bax）was reduced,which enhanced the expression of caspase-3.Combination of ganoderan with Aβ1-40 partially changed the down regulation of bcl-2 expression.The ratio of bcl-2/bax was increased and the expression of caspase-3 was reduced.The neuron protection of ganoderan might be realized through blocking the apoptosis of hippocampus neurons induced by Aβ1-40,by modulating the ratio of bcl-2/bax and by reducing the expression of caspase-3.

关 键 词：灵芝多糖 凋亡 海马神经元 

分 类 号：R965[医药卫生—药理学]