TY -的A2马哈茂德·扎非盟- Naresh阿明,卡兰盟——Rajagru Palanisamy盟——Sarkar Koustav盟,Ganesh m . r . AU -铃木Takayoshi AU -阿里,达乌德盟——Kunka Mohanram,拉姆库玛儿PY - 2021 DA - 2021/04/09 TI -药理激活Nrf2玫红酸变弱的内质网应激在内皮细胞SP - 2732435六世- 2021 AB -内质网(ER)起着关键作用的折叠,修改和贩卖蛋白质。ER的内稳态扰动时,联合国/错误折叠的蛋白质积聚在ER导致ER应激。持续的ER应激导致细胞凋亡,与多种疾病相关。核因子红细胞两个相关因子2 (Nrf2)是一个主要的转录因子在氧化还原内稳态调节多种基因与解毒和对细胞健康有保护作用的机制有关。我们发现,玫红酸(RA)治疗剂量依赖性激活Nrf2使用酶片段互补测定内皮细胞。RA对ER应激的cytoprotective作用内皮细胞凋亡及其分子机制是本研究探讨。Nrf2及其目标基因,以及ER应激标记表达式,是衡量qPCR ER stress-exposed内皮细胞。的贡献Nrf2 RA-mediated防御机制在内皮细胞通过基因敲除研究使用Nrf2-CRISPR / Cas9成立。治疗RA的ER应激激活的内皮细胞表现出Nrf2,证明Nrf2易位和减少ER应激标记。我们发现Nrf2基因敲除激活的内皮细胞对ER压力,并进一步,RA未能调解其cytoprotective效果。 Proteomic studies using LC-MS/MS revealed that among the 1370 proteins detected, we found 296 differentially regulated proteins in ER stress-induced endothelial cells, and RA administration ameliorated 71 proteins towards the control levels. Of note, the ER stress in endothelial cells was attenuated by the treatment with the RA, suggesting the role of the Nrf2 activator in the pathological conditions of ER stress-associated diseases. SN - 1942-0900 UR - https://doi.org/10.1155/2021/2732435 DO - 10.1155/2021/2732435 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -