β 淀粉样肽 (Aβ) 是阿尔茨海默病 (AD) 大脑老年斑中的神经毒性成分。之前我们报道过Aβ毒性是通过诱导音猬因子（SHH）介导的，从而触发细胞周期重入（CCR）和有丝分裂后神经元的凋亡。白花菜是一种蔬菜，其多糖具有免疫调节和抗癌作用，但其对神经退行性变的保护作用从未有报道。在此，我们测试了白巴氏菌衍生的多糖 (PPV-6) 是否可以抑制 Aβ 毒性并探讨其潜在机制。在分化的大鼠皮质神经元中，Aβ25-35 降低了细胞活力，破坏了神经元结构，并损害了线粒体生物能功能，所有这些都被 PPV-6 恢复。免疫细胞化学和蛋白质印迹显示，分化神经元中 Aβ25-35 介导的细胞周期标志物（包括细胞周期蛋白 D1、增殖细胞核抗原 (PCNA) 和 Ser-10 磷酸化组蛋白 H3 (p-Histone H3)）的诱导均被 PPV 抑制-6，同时减少 caspase-3 裂解。进一步的研究表明PPV-6抑制Aβ25-35诱导SHH；事实上，PPV-6 能够抑制由外源音刺猬 N 末端片段 (SHH-N) 引发的神经元 CCR 和细胞凋亡。我们的研究结果表明，在完全分化的神经元中，PPV-6 通过下调 SHH 抑制神经元 CCR 和细胞凋亡，发挥针对 Aβ 神经毒性的保护作用。

The amyloid-beta peptide (Aβ) is the neurotoxic component in senile plaques of Alzheimer's disease (AD) brains. Previously we have reported that Aβ toxicity is mediated by the induction of sonic hedgehog (SHH) to trigger cell cycle re-entry (CCR) and apoptosis in post-mitotic neurons. Basella alba is a vegetable whose polysaccharides carry immunomodulatory and anti-cancer actions, but their protective effects against neurodegeneration have never been reported. Herein, we tested whether polysaccharides derived from Basella alba (PPV-6) may inhibit Aβ toxicity and explored its underlying mechanisms. In differentiated rat cortical neurons, Aβ25-35 reduced cell viability, damaged neuronal structure, and compromised mitochondrial bioenergetic functions, all of which were recovered by PPV-6. Immunocytochemistry and western blotting revealed that Aβ25-35-mediated induction of cell cycle markers including cyclin D1, proliferating cell nuclear antigen (PCNA), and histone H3 phosphorylated at Ser-10 (p-Histone H3) in differentiated neurons was all suppressed by PPV-6, along with mitigation of caspase-3 cleavage. Further studies revealed that PPV-6 inhibited Aβ25-35 induction of SHH; indeed, PPV-6 was capable of suppressing neuronal CCR and apoptosis triggered by the exogenous N-terminal fragment of sonic hedgehog (SHH-N). Our findings demonstrated that, in the fully differentiated neurons, PPV-6 exerts protective actions against Aβ neurotoxicity via the downregulation of SHH to suppress neuronal CCR and apoptosis.