RETRACTED: Astragalus polysaccharide alleviates H2O2-triggered oxidative injury in human umbilical vein endothelial cells via promoting KLF2 (Retracted Article)

被引：22

作者：

Li, Dongtao ^{[1
]}

Liu, Yan ^{[1
]}

Xu, Rong ^{[1
]}

Jia, Xin ^{[1
]}

Li, Xing ^{[1
]}

Huo, Cong ^{[1
]}

Wang, Xiaoming ^{[1
]}

机构：

[1] Fourth Mil Med Univ, Dept Geriatr, Xijing Hosp, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China

来源：

ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY | 2019年 / 47卷 / 01期

关键词：

Astragalus polysaccharide; vascular dysfunction; KLF2; H2O2; MEK/ERK; STRESS; DYSFUNCTION; APOPTOSIS; OXYGEN; ROLES; ACTIVATION; MECHANISM; PROTECTS; MEK/ERK; PATHWAY;

D O I：

10.1080/21691401.2019.1621886

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The damage of vascular endothelial cells has become an indispensable factor in the occurrence and advancement of cardiovascular diseases. In the current study, we investigated the effect of Astragalus Polysacharin (APS) on H2O2-evoked oxidative injury in HUVECs. HUVECs cells were treated by H2O2 to induce oxidative damage. Cells viability, apoptosis and reactive oxygen species (ROS) level were detected through CCK8 assay and flow cytometry. The cell growth-related proteins and heme oxygenase- 1(HO-1) and KLF2 expression were evaluated via Western blot assay. The functions of KLF2 in APS and H2O2 co-disposed HUVECs were explored after si-KLF2 transfection. MEK/ERK pathway was finally measured through Western blot. We found that H2O2 stimulation-evoked HUVECs oxidative damage meanwhile impeded HO-1 expression. APS treatment effectively suppressed H2O2-induced oxidative injury in HUVECs. KLF2 and Nrf2 expression were elevated by APS and KLF2 repression abolished the protective action of APS in H2O2-triggered cell injury. MEK/ERK pathway was activated by APS treatment. Furthermore, the MEK/ERK pathway inhibitor weakened the promoting effect of APS on the expression of KLF2. In conclusion, our study reveals that APS alleviates H2O2-triggered oxidative injury in HUVECs via elevating the expression of KLF2 via the MEK/ERK pathway.

引用

页码：2188 / 2195

页数：8