Proteomic analysis of ginsenoside Re attenuates hydrogen peroxide-induced oxidative stress in human umbilical vein endothelial cells
Proteomic analysis of ginsenoside Re attenuates hydrogen peroxide-induced oxidative stress in human umbilical vein endothelial cells
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DOI：
10.1039/c6fo00123h
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发表时间：
2016-01-01
期刊：
影响因子：
6.1
通讯作者：
Zeng, Rong
中科院分区：
文献类型：
--
作者：
Huang, Gui-dong;Zhong, Xian-feng;Zeng, Rong
人参皂苷Re是人参中的一种活性成分，因其对心血管系统具有明显的治疗作用而备受关注。然而，很少有基本的信息是可利用的机制和药理学作用的阿托伐他汀。本研究探讨Re对H2O2诱导的人脐静脉内皮细胞（HUVECs）氧化损伤的保护作用及其可能机制。采用H2O2建立氧化损伤模型。采用MTT法、抗氧化指示剂法等一系列实验方法研究Re的抗氧化作用。从蛋白质组学水平探讨Re的保护机制，并通过实时定量PCR和Western blotting对差异表达蛋白进行验证。结果表明Re可能是一种潜在的抗氧化剂，可以保护HUVECs免受氧化应激损伤。蛋白质组学分析表明，Re和H2O2处理组中有23个蛋白质点表达上调以抵抗氧化应激，其中15个蛋白质点通过质谱鉴定。这些上调的蛋白质参与应激反应、抗氧化系统、蛋白质合成、转录和翻译后修饰的调节以及线粒体功能的修复。本研究可能为探讨利多卡因保护心血管系统的作用机制提供新的思路。
Ginsenoside Re is an active component in ginseng that has attracted much attention because of its evident therapeutic effects on the cardiovascular system. However, little basic information is available on the mechanisms and pharmacological effects of ginsenoside Re. The potential mechanisms and protective effects of Re on H2O2-induced oxidative injury in human umbilical vein endothelial cells (HUVECs) were investigated in this study. An oxidative injury model was established using H2O2. The anti-oxidative effects of Re were determined using a series of experiments, such as MTT and anti-oxidative indicator assays. The potential protective mechanisms of Re were explored at the proteomic level, and differentially expressed proteins were validated by quantitative real-time polymerase chain reaction and western blotting. Results indicated that Re could be a potential anti-oxidant to protect HUVECs against oxidative stress damage. Proteomic analysis showed that the expression of 23 protein spots was upregulated in Re and H2O2 groups to resist oxidative stress, 15 of which were identified by their mass spectrum. These upregulated proteins were involved in stress response, anti-oxidative systems, protein synthesis, regulation of transcription and post-translational modifications, and repair of mitochondrial functions. This study may provide new insights into the mechanisms of ginsenoside Re in protecting the cardiovascular system.