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 onβamyloid protein-induced injury in cells

作　　者：王婷[1,2] 李乐迅 邵长胜 周富丁 赵涵瑜 李亚楠 谢必果 王鹏 陈文军[1] WANG Ting;LI Le-Xun;SHAO Chang-Sheng;ZHOU Fu-Ding;ZHAO Han-Yu;LI Ya-Nan;XIE Bi-Guo;WANG Peng;CHEN Wen-Jun(School of Public Health,Anhui Medical University,Hefei 230031,China;Xueyan Town Central Health Center,Changzhou 213000,China;Key Laboratory of High Magnetic Field and Ion Beam Physical Biology,Hefei Institutes of Physical Science,Chinese Academy of Sciences,Hefei 230031,China)

机构地区：[1]安徽医科大学公共卫生学院,合肥230031 [2]雪堰镇中心卫生院,常州213000 [3]中国科学院合肥物理科学研究院,强磁场与离子束物理生物学重点实验室,合肥230031

出　　处：《食品安全质量检测学报》2024年第19期155-164,共10页Journal of Food Safety and Quality

摘　　要：目的探讨黄精多糖(Polygonatum sibiricum polysaccharides,PSP)对β淀粉样蛋白(25-35)[βamyloid protein(25-35),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。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。Objective To investigate the protective effects of Polygonatum sibiricum polysaccharides(PSP)on cell oxidative damage and apoptosis induced byβamyloid protein(25-35)(Aβ_(25-35))and to further explore the neuroprotective effect of PSP and its potential mechanisms.Methods The intervention concentration and time of Aβ_(25-35)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 Aβ_(25-35)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.

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 

分 类 号：R749.16[医药卫生—神经病学与精神病学] TS201.4[医药卫生—临床医学]