紫草宁通过PI3K/Akt通路抑制百草枯诱导的SH-SY5Y细胞损伤  

Shikonin Inhibits Paraquat-induced SH-SY5Y Cell Injury through PI3K/Akt Activation

作　　者：吕艳霞[1] 赵丹[1] 张志锋[1] 

机构地区：[1]湖北医药学院基础医学院生理学教研室,湖北十堰442000

出　　处：《湖北医药学院学报》2017年第2期120-123,128,共5页Journal of Hubei University of Medicine

基　　金：湖北省教育厅科学研究计划指导性项目(B2015492);十堰市科学技术研究与开发项目(16Y07);湖北医药学院研究生启动金(2010QDJ13)

摘　　要：目的:探讨紫草宁对SH-SY5Y细胞在百草枯诱导的帕金森(PD)样损伤模型中的作用效果及机制。方法:SH-SY5Y细胞经紫草宁提前处理1 h,与百草枯(1 mmol/L)和/或LY294002(1μmol/L)共处理24 h,MTT法检测细胞活性大小,Western blotting检测p-Akt(Ser 473)水平变化。结果:中、高浓度的紫草宁可降低百草枯诱导的SH-SY5Y死亡率,同时可提高细胞p-Akt(Ser 473)水平;LY294002可抑制紫草宁对细胞p-Akt水平和死亡率的影响。结论:一定浓度的紫草宁可经PI3K途径激活SH-SY5Y细胞Akt活性,可减弱百草枯诱导的细胞损伤。Objective To explore the effect of and mechanism of shikonin on SH-SY5Y cells derived from paraquat-induced Parkinson＇s disease （PD） model. Methods SH-SY5Y cells were pretreated with Shikonin for 1 hour and then treated with paraquat （ 1 mmol / L） and/or LY294002 （ 1 μmol/L） for 24 h. Then cell viability and p-Akt （ ser 473） level were measured by MTT and western blotting respectively.Results Middle and high concentration of shikonin decreased paraquat-in- duced SH-SY5Y cell death and increased the level of p-Akt. LY294002 could reduce shikonin-induced p-Akt elevation and attenuate the effect of shikonin on the cell death rate in the injury model Conclusion A certain concentration of shikonin could inhibit paraquat-indueed oxidative stress injury through the activation of PI3K/Akt pathway.

关 键 词：紫草宁 百草枯 帕金森 氧化应激 SH-SY5Y Akt 

分 类 号：R285[医药卫生—中药学]