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首页|期刊导航|湖北医药学院学报|紫草宁通过PI3K/Akt通路抑制百草枯诱导的SH-SY5Y细胞损伤

紫草宁通过PI3K/Akt通路抑制百草枯诱导的SH-SY5Y细胞损伤

吕艳霞 赵丹 张志锋

湖北医药学院学报2017,Vol.36Issue(2):120-123,128,5.
湖北医药学院学报2017,Vol.36Issue(2):120-123,128,5.DOI:10.13819/j.issn.1006-9674.2017.02.006

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

吕艳霞 1赵丹 1张志锋1

作者信息

  • 1. 湖北医药学院基础医学院生理学教研室,湖北十堰442000
  • 折叠

摘要

Abstract

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.Rtesults Middle and high concentration of shikonin decreased paraquat-induced 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-induced 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

Key words

Shikonin/Paraquat/Parkinson's disease/Oxidative stress/SH-SY5Y/Akt

引用本文复制引用

吕艳霞,赵丹,张志锋..紫草宁通过PI3K/Akt通路抑制百草枯诱导的SH-SY5Y细胞损伤[J].湖北医药学院学报,2017,36(2):120-123,128,5.

基金项目

湖北省教育厅科学研究计划指导性项目(B2015492) (B2015492)

十堰市科学技术研究与开发项目(16Y07) (16Y07)

湖北医药学院研究生启动金(2010QDJ13) (2010QDJ13)

湖北医药学院学报

2096-708X

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