天麻素保护过氧化氢诱导的神经元氧化损伤的研究

Study on gastrodin protects neuron from hydrogen peroxide-induced oxidative damage

目的:探究天麻素对过氧化氢引起的神经细胞氧化损伤的保护作用及其作用机制。方法:培养SH-SY5Y细胞,并分为3组:对照组、氧化损伤组和天麻素处理组。用流式细胞术检测细胞凋亡率及细胞活性氧(ROS)水平,用ELISA检测细胞内超氧化物歧化酶(SOD)表达水平,用蛋白质免疫印迹实验检测细胞内PI3K、AKT磷酸化水平。结果:过氧化氢处理引起细胞凋亡率升高,胞内ROS平上升,SOD表达下调以及PI3K、AKT磷酸化水平下降;天麻素处理后可以显著抑制过氧化氢引起的细胞凋亡、ROS水平上升及SOD表达下调,并缓解氧化损伤对PI3K/AKT磷酸化的抑制作用。结论:天麻素通过激活PI3K/AKT信号通路保护过氧化氢诱导的神经细胞氧化损伤。

Objective:To investigate the effect of gastrodin on hydrogen peroxide-induced neuron oxidative damage,and to reveal the mechanism.Methods:Human neuroblastoma cell line SH-SY5Y was cultured and divided into three groups:control group,oxidative damage group and gastrodin treated group.The apoptotic cells and the reactive oxygen species were detected by flow cytometry;the SOD expression level was measured by ELISA assay;the phosphorylations of PI3K and AKT were measured by Western blot.Results:Hydrogen peroxide-induced oxidative damage caused cell apoptosis and ROS burst,while SOD expression level and PI3K/AKT phosphorylation were decreased.Gastrodin treatment decreased cell apoptosis rate and ROS levels,and reduced the inhibitory effects on PI3K/AKT phosphorylation by oxidative damage.Conclusion:Gastrodin protects neuron from hydrogen peroxide-induced oxidative damage via PI3K/AKT signaling pathway.