中文摘要：

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（PCI2细胞）神经毒性的抑制作用和潜在机制。方法将PCI2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PCI2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PCI2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βcatenin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一3B信号蛋白的活化。结论淫羊藿苷可显著抑制Aβ25-35所致的PCI2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。

英文摘要：

OBJECTIVE To investigate the neuroprotective effects of icariin on Aβ25-35 induced cytotoxicity in PC12 cells and its potential mechanism. METHODS Control, AI325.35 treatment, A~25.3Jicariin combination treatment and icariin single treatment groups were set.Aβ25-35 was used to induce eytotoxicity in PC12 cells, and the neuroproteetive effects of ieariin were investigated. RE- SULTS Icariin significantly inhibited Aβ25-35-induced neurotoxicity and apoptosis-related protein（caspase-3 and PARP）expressions. Mechanism study showed that icariin significantly activated 13-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.