氧化应激
富马酸二甲酯
视网膜
化学
KEAP1型
背景(考古学)
细胞生物学
银屑病
激活剂(遗传学)
抗氧化剂
细胞内
体外
生物化学
药理学
免疫学
医学
生物
多发性硬化
受体
转录因子
古生物学
基因
作者
Federico Manai,Marialaura Amadio
出处
期刊:Antioxidants
[MDPI AG]
日期:2022-09-28
卷期号:11 (10): 1924-1924
被引量:7
标识
DOI:10.3390/antiox11101924
摘要
Dimethyl fumarate (DMF) is a well-known activator of Nrf2 (NF-E2-related factor 2), used in the treatment of psoriasis and multiple sclerosis. The mechanism of action consists in the modification of the cysteine residues on the Nrf2-inhibitor Keap1, thus leading to the dissociation of these two proteins and the consequent activation of Nrf2. Considering the paucity of evidence of DMF effects in the context of retinal endothelium, this in vitro study investigated the role of DMF in human retinal endothelial cells (HREC). Here, we show for the first time in HREC that DMF activates the Nrf2 pathway, thus leading to an increase in HO-1 protein levels and a decrease in intracellular ROS levels. Furthermore, this molecule also shows beneficial properties in a model of hyperglucose stress, exerting cytoprotective prosurvival effects. The overall collected results suggest that DMF-mediated activation of the Nrf2 pathway may also be a promising strategy in ocular diseases characterized by oxidative stress. This study opens a new perspective on DMF and suggests its potential repositioning in a broader therapeutical context.
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