Quercetin inhibits the amphiregulin/EGFR signaling‐mediated renal tubular epithelial‐mesenchymal transition and renal fibrosis in obstructive nephropathy

安非雷古林 纤维化 槲皮素 癌症研究 转化生长因子 表皮生长因子受体 氧化应激 化学 上皮-间质转换 细胞凋亡 药理学 医学 内科学 受体 生物化学 癌症 抗氧化剂 转移
作者
Qi Wang,Fuqiang Wang,Xiangze Li,Zhi Ma,Dapeng Jiang
出处
期刊:Phytotherapy Research [Wiley]
卷期号:37 (1): 111-123 被引量:9
标识
DOI:10.1002/ptr.7599
摘要

Abstract Quercetin is a widely distributed, bioactive flavonoid compound, which displays potential to inhibit fibrosis in several diseases. The purpose of our study was to determine the effect of quercetin treatment on renal fibrosis and investigate the mechanism. Human proximal tubular epithelial cells (HK‐2) stimulated by transforming growth factor‐β1 (TGF‐β1) and a rat model of unilateral ureter obstruction (UUO) that contributes to fibrosis were used to investigate the role and molecular mechanism of quercetin. PD153035 ( N ‐[3‐Bromophenyl]‐6,7‐dimethoxyquinazolin‐4‐amine) was used to inactivate EGFR (epidermal growth factor receptor). The level of fibrosis, proliferation, apoptosis, and oxidative stress in HK‐2 were measured. All data are presented as means ± standard deviation (SD). p ‐value < .05 was considered statistically significant. In UUO rats, quercetin reduced the area of fibrosis as well as inflammation, oxidative stress, and cell apoptosis. In cultured HK‐2 cells, quercetin significantly ameliorated the EMT induced by TGF‐β1, which was accompanied by increased amphiregulin (AREG) expression. Moreover, quercetin inhibited AREG binding to the EGFR receptor, thereby further affecting other downstream pathways. Quercetin may alleviate fibrosis in vitro and in vivo by inhibiting the activation of AREG/EGFR signaling indicating a potential therapeutic effect of quercetin in renal fibrosis.
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