【摘要】 目的研究不同剂量的染料木黄酮(Gen)对β淀粉样肽25-35(Aβ25-35)介导的PC12细胞凋亡的保护作用,并探讨了可能的分子调控机制。方法PC12细胞传代培养48 h后,选取生长良好的同批次细胞,随机分为5组,即对照组、Aβ模型组(20μmol/L)、Gen干预组(25、50和100μmol/L)。Gen预处理2 h后,经Aβ25-35染毒,建立细胞损伤模型;24 h后,收集细胞,用逆转录-聚合酶链反应(RT-PCR)法检测PC12细胞caspase-3、caspase-9、bcl-xl、bad和LRP5基因的表达。结果与对照组相比,Aβ组细胞caspase-3、caspase-9和bad mRNA表达上调,其差异具有统计学意义(P<0.05),bcl-xl、LRP5 mRNA表达下调,差异具有统计学意义(P<0.05);与Aβ组相比,Gen高剂量组可显著下调PC12细胞caspase-3、caspase-9和bad mRNA表达(P<0.05);Gen高剂量组可显著上调bcl-xl、LRP5 mRNA,差异有统计学意义(P<0.01)。结论 Gen可能是通过下调细胞凋亡促进基因caspase-3、caspase-9和bad mRNA表达,上调细胞凋亡抑制基因bcl-xl、LRP5 mRNA表达,拮抗Aβ诱导的神经细胞凋亡,从而发挥神经细胞保护作用。更多还原

【Abstract】 Objective To study the protective effects of genistein(Gen) on the apoptosis of PC12 cells induced by beta amyloid 25-35(Aβ 25-35) and its possible mechanism.Methods PC12 cells were divided into control group,Aβ 25-35 group,and 3 Gen groups(at the dosage of 25,50 and 100 μmol/L).After pre-incubated with or without Gen for 2 h,PC12 cells were exposed to 20 μmol of Aβ 25-35 for 24 h.The relative expression of β-actin,caspase-3,caspase-9,bad,bcl-xl and LRP5 mRNA in PC12 cells were analyzed by RT-PCR.Results Compared with the Aβ treated group,the expression of caspase-3,caspase-9 and bad mRNA were significantly decreased(P < 0.05),but the expression of bcl-xl,LRP5 mRNA were significantly increased(P < 0.05) in the high dose Gen group.Conclusion The neuroprotection of Gen on PC12 cells against apoptosis induced by Aβ 25-35 might be the effect of down-regulating the expression of caspase-9,caspase-3 and bad mRNA,and up-regulating the expression of bcl-xl,LRP5 mRNA.更多还原