摘要
目的:探讨克癃胶囊对H_2O_2刺激前列腺癌细胞(PC-3)引起的氧化应激反应的保护作用和分子机制。方法:通过H_2O_2作用于PC-3细胞建立氧化应激的损伤模型;利用流式细胞仪技术、化学显色法分别检测细胞内活性氧(ROS)、还原型谷胱甘肽(GSH)含量;Western Blot和RT-PCR检测细胞Nrf2通路相关因子蛋白和mRNA的表达变化。结果:克癃胶囊能降低细胞内由H_2O_2引起的ROS升高(P<0.01),升高由H_2O_2引起的GSH降低(P<0.01);Western Blot结果显示,加入克癃胶囊干预后Nrf2、COX-2、HO-1、NQO1蛋白表达均增强(P<0.01);RT-PCR结果显示,克癃胶囊干预后Nrf2、COX-2、HO-1、NQO1 mRNA水平表达明显增强(P<0.05)。结论:克癃胶囊对H_2O_2引起PC-3细胞的氧化应激具有保护作用,其作用机制是通过调控Nrf2通路,激活体内抗炎抗氧化机制而实现的。
Objective：To explore the protective effect and molecular mechanism of Kelong Capsules（KLC） on the oxidative stress induced by hydrogen peroxide stimulation of PC-3 cells.Methods：Oxidative stress damage model of PC-3 cells was established by hydrogen peroxide stimulation.Contents of intracellular ROS and GSH were detected by flow cytometry and chemical coloration method respectively.Nrf2 signaling pathway related protein and mRNA expression were detected by Western Blot and RT-PCR respectively.Results：KLC pretreatment significantly decreased ROS levels and increased intracellular GSH content induced by hydrogen peroxide（P〈0.01）.Additionally,KLC pretreatment obviously increased the expression of Nrf2 signaling pathway relating protein and mRNA such as COX-2,HO-1 and NQO1（P〈0.01,P〈0.05）.Conclusion：KLC showed certain protective effect on PC-3 cells from hydrogen peroxide-inducedoxidative stress,which may be partly due to increasing the expression of the Nrf2 signaling pathway related protein and genes.
作者
全丹妮
谢辉
张玲
颜苗
樊新荣
QUAN Dan-ni;XIE Huil;ZHANG Ling;YAN Miao;FAN Xin-Rong(Hunan University of Chinese Medicine, Changsha 410208, China;Department of Pharmacy, The Second Xiangya Hospital of Central South University, Institute of Clinical Pharmacy, Central South University, Changsha 410011, China;China Academy of Chinese Medical Sciences, Beijing 100700, China)
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2018年第2期679-682,共4页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家自然科学基金项目(No.81373708,No.81573686)
关键词
克癃胶囊
Nrf2信号通路
过氧化氢
氧化应激
Kelong Capsule
Nrf2 signaling pathway
Hydrogen peroxide
Oxidative stress
