TRPM2型
细胞凋亡
炎症
聚ADP核糖聚合酶
脂多糖
药理学
脂质过氧化
活性氧
医学
过氧亚硝酸盐
线粒体ROS
程序性细胞死亡
氧化应激
免疫学
癌症研究
细胞生物学
化学
生物
生物化学
内分泌学
内科学
瞬时受体电位通道
受体
聚合酶
基因
酶
超氧化物
作者
Hatice Daldal,Mustafa Nazıroğlu
标识
DOI:10.1080/09273948.2022.2075400
摘要
Purpose We investigated the possible protective effects of rituximab (RTX) on LPS-induced oxidant, inflammatory, and apoptotic adverse actions via the inhibition of TRPM2 channel in the adult retinal pigment epithelial-19 (ARPE-19) cells.Methods In the cultured ARPE-19 cells, we induced five main groups as control, RTX (10 μg/ml), LPS (1 μg/ml), LPS+RTX, and LPS+TRPM2 blockers (ACA or 2/APB).Results The levels of apoptosis, cell death, mitochondrial free reactive oxygen radicals (mitROS), cytosolic ROS, lipid peroxidation, caspase −3, caspase −8, caspase −9, ADP-ribose-induced TRPM2 current density, TNF-α, IL-1β, cytosolic free Zn2+, and Ca2+ were increased by LPS, although their levels were diminished by the treatments of RTX and TRPM2 blockers.Conclusions The LPS-induced mitROS, inflammatory cytokine, and apoptosis levels were modulated via TRPM2 inhibition in the human retinal epithelial cells by the RTX treatment. The RTX may be considered as a new therapeutic approach to LPS-induced human retinal epithelial cell injury.
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