灯盏乙素调节ATP敏感性钾通道对抗β-淀粉样蛋白的毒性作用  

Scutellarin inhibits β-amyloid peptide-induced toxicity by ATP-sensitive potassium channel in vitro

作　　者：王宁慧 伍棋 于燕妮[1] 郭莉莉 WANG Ning-Hui;WU Qi;YU Yan-Ni(Guizhou Medical University, Guiyang 550004, Guizhou, China)

机构地区：[1]贵州医科大学,贵州贵阳550004 [2]贵阳市第一人民医院

出　　处：《中国老年学杂志》2019年第12期2972-2976,共5页Chinese Journal of Gerontology

基　　金：国家自然科学基金项目(30870986);贵州省科学技术基金项目(黔科合J字[2012]2091号)

摘　　要：目的观察灯盏乙素(Scu)对β-淀粉样蛋白(Aβ)1~42诱导的细胞模型中ATP敏感性钾(KATP)通道的影响,探讨其对抗Aβ毒性损害的作用机制。方法将神经母细胞瘤细胞分为对照组、Scu处理组、Aβ处理组、Scu+Aβ处理组及二氮嗪(DZ)+Aβ处理组,用生物化学方法检测各组细胞内的ATP含量;用Western印迹法检测各组细胞中KATP通道亚基Kir6.1、Kir6.2、SUR1、SUR2的蛋白表达情况;用荧光探针定量法检测各组细胞的细胞膜和线粒体膜膜电位变化;用流式细胞术测定各组细胞总凋亡率。结果与对照组和Scu处理组相比,Aβ处理组细胞中的ATP含量明显降低(P<0.01),Kir6.1和SUR2的蛋白表达上调(P<0.01),细胞膜和线粒体膜膜电位去极化(P<0.05),细胞总凋亡率增加(P<0.01),Scu的干预调节了上述指标趋向于正常。DZ+Aβ处理组的各指标变化与Scu+Aβ处理组基本一致。结论Scu能够调控ATP介导的Kir6.1/SUR2亚基KATP通道的开放来抑制Aβ毒性所致的细胞凋亡,从而发挥神经元保护作用。Objective To investigate the effect of scutellarin (Scu) on ATP-sensitive potassium (KATP)channel in cell model, and to explore the mechanism for reducing Aβ toxicity damage. Methods SH-SY5Y cells were divided into control, Scu treatment, Aβ treatment, Aβ+Scu treatment, and Aβ+DZ treatment groups. The content of ATP was determined by biochemical method. The expressions of Kir6.1, Kir6.2, SUR1, SUR2 were examined by Western blot. Cell membrane potential was detected by fluorescence probe DiBAC4(3) and mitochondrial membrane potential was examined by JC-1. Apoptotic rate was detected by flow cytometry. Results Compared with that of control group and Scu treatment group, the content of ATP was obviously reduced( P <0.05), the protein expressions of Kir6.1 and SUR2 were increased( P <0.05), cell membrane potential and mitochondrial membrane potential were decreased( P <0.05), and apoptotic rate was increased in Aβ treatment cells( P <0.05). The interventions of Scu regulated the above indicators tending to normal. The changes of all above indicators of the cells treating with Aβ+DZ were almost the same as treating with Aβ+Scu. Conclusions Scu could adjust Kir6.1/SUR2 KATP channel opening by ATP mediated to inhibit Aβ 1~42 -induced cell apoptosis, and to exert protective action of neuron.

关 键 词：灯盏乙素 Β淀粉样蛋白 ATP敏感性钾通道 神经母细胞瘤细胞 

分 类 号：R361[医药卫生—病理学]