Arctiin ameliorates advanced oxidation protein product-induced epithelial-to- mesenchymal transition in HK-2 cells by inhibiting endoplasmic reticulum stress.
- Author:
Jun ZHANG
1
;
Li-Li HUANG
;
Xiu-Jie LIANG
;
Yue WANG
;
Na DUAN
;
Xiao-Hong XIANG
;
Shuang-Shuang SHU
;
Ting-Ting GUO
;
Lei YANG
;
Xun TANG
Author Information
- Publication Type:Journal Article
- MeSH: Advanced Oxidation Protein Products; adverse effects; Cadherins; metabolism; Cell Line; Endoplasmic Reticulum Stress; Epithelial Cells; cytology; drug effects; Epithelial-Mesenchymal Transition; Furans; pharmacology; Glucosides; pharmacology; Heat-Shock Proteins; metabolism; Humans; Kidney Tubules; cytology; drug effects; Oxidative Stress; Reactive Oxygen Species; metabolism; Vimentin; metabolism
- From: Journal of Southern Medical University 2016;36(6):833-837
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of arctiin on advanced oxidation protein product (AOPP)-induced epithelial-to-mesenchymal transition (EMT) in tubular cells and explore the mechanisms underlying this effect.
METHODSHuman proximal tubular cells (HK-2 cells) were treated with bovine serum albumin (BSA) or AOPPs in the presence or absence of arctiin. The expressions of E-cadherin, vimentin, and GRP78 at the protein and mRNA levels in the cells were examined using Western blotting and quantitative real-time PCR. The level of reactive oxygen species (ROS) was measured by flow cytometry with DCFH-DA as the fluorescent probe.
RESULTSCompared with BSA-treated cells, the cells treated with AOPPs showed decreased expression of epithelial cell marker E-cadherin and overexpression of mesenchymal marker vimentin and endoplasmic reticulum stress marker GRP78 with an increased ROS level. These changes induced by AOPPs were partly inhibited by arctiin.
CONCLUSIONArctiin can ameliorate AOPP-induced EMT in tubular cells by inhibiting endoplasmic reticulum stress, and oxidative stress response may participate in this process.