黄精多糖对β淀粉样蛋白诱导细胞损伤的保护作用及机制研究

Study of protective effect and mechanism of Polygonatum sibiricum polysaccharides on β amyloid protein-induced injury in cells

中文关键词:  黄精多糖  β淀粉样蛋白（25-35）  氧化应激  线粒体功能  细胞凋亡

英文关键词:Polygonatum sibiricum polysaccharides  β amyloid protein（25-35）  oxidative stress  mitochondrial function  cell apoptosis

中文摘要:

      目的：探讨黄精多糖 (Polygonatum sibiricum polysaccharides, PSP)对Aβ_25-35诱导的SH-SY5Y细胞氧化损伤及凋亡的神经保护作用及其机制。方法：通过CCK-8实验确定Aβ_25-35和PSP的干预浓度和时间,并将细胞分为对照组、模型组、低、中、高剂量组。检测细胞的凋亡、线粒体膜电位(Mitochondrial membrane potential, MMP)水平、细胞色素C(Cytochrome C, Cyt C)含量、胞内活性氧(Reactive oxygen species, ROS)含量以及多种抗氧化酶活性变化。之后采用蛋白质印迹法(Western blot, WB)实验检测Nrf2/HO-1和JAK2/STAT3信号通路相关蛋白表达。结果：与模型组相比,PSP能够显著恢复细胞活力,清除胞内ROS,升高细胞MMP,减少线粒体Cyt C释放,抑制凋亡蛋白的生成。同时能够逆转Aβ_25-35对Nrf2/HO-1信号通路的抑制,降低 JAK2/STAT3通路的磷酸化程度。结论： PSP可通过上调Nrf2/HO-1信号通路相关蛋白分子的表达,逆转JAK2/STAT3信号通路的磷酸化,减轻氧化损伤,改善线粒体功能并最终抑制细胞凋亡。

英文摘要:

      Objective To investigate the protective effects of Polygonatum sibiricum polysaccharides (PSP) on cell oxidative damage and apoptosis induced by Aβ25-35 and to further explore the neuroprotective effect of PSP and its potential mechanisms. Methods The intervention concentration and time of Aβ25-35 and PSP were determined by CCK-8 assay, and the cells were divided into control group, model group, low, medium and high dose groups. The apoptosis, mitochondrial membrane potential (MMP) level, cytochrome C (Cyt C) content, reactive oxygen species (ROS) and activity of antioxidant enzymes were detected. Protein expression levels of Nrf2/HO-1 and JAK2/STAT3 signaling pathways were detected by western blot (WB). Results Compared with the model group, PSP could significantly restore cell vitality, clear intracellular ROS, increase MMP, reduce mitochondrial Cyt C release, and inhibit apoptotic protein production. At the same time, it could reverse the inhibition of Aβ25-35 on Nrf2/HO-1 signaling pathway and reduce the phosphorylation degree of JAK2/STAT3 pathway. Conclusion PSP can play a neuroprotective role by up-regulating the expression of protein molecules related to Nrf2/HO-1 signaling pathway, reversing the phosphorylation of JAK2/STAT3 signaling pathway, alleviating oxidative damage, improving mitochondrial function and ultimately inhibiting apoptosis.