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红景天苷对H2O2诱导的人晶状体上皮细胞氧化应激损伤的保护作用

刘礼婷 郑文韬 刘平 张丽娟

国际眼科杂志2017,Vol.17Issue(10):1834-1836,3.
国际眼科杂志2017,Vol.17Issue(10):1834-1836,3.DOI:10.3980/j.issn.1672-5123.2017.10.07

红景天苷对H2O2诱导的人晶状体上皮细胞氧化应激损伤的保护作用

The protection of salidroside on oxidative stress induced in human lens epithelium cells

刘礼婷 1郑文韬 1刘平 1张丽娟1

作者信息

  • 1. 150001 中国黑龙江省哈尔滨市,哈尔滨医科大学附属第一医院眼科
  • 折叠

摘要

Abstract

AIM:To explore the effect of different concentrations of salidroside on H2 O2 induced oxidative stress damage in human lens epithelium cells ( HLEC) . · METHODS: HLEC were cultured and divided into negative control group: cultured in normal cultivation;oxidative damage group: treated with 100μmol/L H2 O2 for 12h; Salidroside low concentration group: 10μmol/L salidroside treated for 24h and H2 O2 treated for 12h;Salidroside high concentration group: 100μmol/L salidroside treated for 24h and H2 O2 treated for 12h. MTT method was applied to observe the effect of salidroside on HLEC survival rate. Morphological change of each group were observed and recorded under inverted microscope. DCFH-DA fluorescent probe was applied to detect intracellular ROS changes; content of malondialdehyde ( MDA ) , superoxide dismutase ( SOD ) and glutathione peroxidase ( GSH-Px ) in supernatants were detected by pectrophotometer. · RESULTS: Salidroside obviously inhibited H2 O2 -induced HLEC vitality decline, inhibited ROS generation in cells, causing SOD, GSH-Px levels increased and MDA levels decreased. ·CONCLUSION:Salidroside inhibited H2 O2 induced HLEC injury by decreasing the intracellular MDA content levels and increasing SOD, GSH-Px content levels, which conclude that salidroside may have a certain role in the treatment of HLEC damage.

关键词

红景天苷/过氧化氢/晶状体上皮细胞/保护

Key words

salidroside/hydrogen peroxide/human lens epithelium cell/protect

引用本文复制引用

刘礼婷,郑文韬,刘平,张丽娟..红景天苷对H2O2诱导的人晶状体上皮细胞氧化应激损伤的保护作用[J].国际眼科杂志,2017,17(10):1834-1836,3.

基金项目

国家自然科学基金面上项目(No. 30973275)The National Natural Science Foundation ( No. 30973275) (No. 30973275)

国际眼科杂志

OA北大核心CSTPCD

1672-5123

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