【摘要】 目的研究淫羊藿苷(icariin)对β-淀粉样蛋白(Aβ25-35)所致的大鼠肾上腺嗜铬细胞瘤细胞株(PC12细胞)神经毒性的抑制作用和潜在机制。方法将PC12细胞分为正常对照组、Aβ25-35损伤组、淫羊藿苷与Aβ25-35共同给药组、淫羊藿苷单独给药组,然后考察淫羊藿苷对PC12细胞损伤的保护作用,以及淫羊藿苷对Wnt/β-catenin信号通路的调节作用。结果淫羊藿苷可以显著的抑制Aβ25-35所诱导的PC12细胞神经毒性,提高细胞存活率,此外其还可以降低凋亡相关蛋白caspase-3和PARP的激活。机制研究发现,淫羊藿苷可以激活Wnt/β-catenin信号通路中的关键蛋白β-catenin的活性,抑制其磷酸化,并促进该蛋白向细胞核中的转运。此外,淫羊藿苷还可以通过调节不同的磷酸化位点来抑制GSK-3β信号蛋白的活化。结论淫羊藿苷可显著抑制Aβ25-35所致的PC12细胞的毒性作用,其潜在机制可能是通过激活Wnt/β-catenin信号通路来实现的。更多还原

【Abstract】 OBJECTIVE To investigate the neuroprotective effects of icariin on Aβ25-35-induced cytotoxicity in PC12 cells and its potential mechanism.METHODS Control,Aβ25-35 treatment,Aβ25-35/icariin combination treatment and icariin single treatment groups were set.Aβ25-35 was used to induce cytotoxicity in PC12 cells,and the neuroprotective effects of icariin were investigated.RESULTS Icariin significantly inhibited Aβ25-35-induced neurotoxicity and apoptosis-related protein(caspase-3 and PARP)expressions.Mechanism study showed that icariin significantly activated β-catenin protein by promoting β-catenin dephosphorylation and nuclear translocation.In addition,icariin also inhibited GSK-3β activation by regulating different phosphorylation sites.CONCLUSION Icariin can effectively inhibit Aβ25-35-induced cytotoxicity in PC12 cells via Wnt/β-catenin signaling pathway.更多还原