文献类型：期刊文献

英文题名：One-electron reduction triggered nitric oxide release for ischemia-reperfusion protection

作者：Xu, Xiu[1];Sun, Meiling[2];Luo, Xiao[3];Zhang, Ziqian[4];Su, Lin[1];Cui, Lingfei[5];Zhu, Zhihui[2];Lu, Xicun[1];Wang, Rui[1];Han, Feng[2];Qian, Xuhong[1];Yang, Youjun[1]

机构：[1]East China Univ Sci & Technol, Shanghai Key Lab Chem Biol, Sch Pharm, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Nanjing Med Univ, Sch Pharm, Key Lab Cardiovasc & Cerebrovasc Med, Nanjing 211166, Peoples R China;[3]East China Normal Univ, Sch Chem & Mol Engn, Dongchuan Rd 500, Shanghai 200241, Peoples R China;[4]Guangxi Univ Chinese Med, Guangxi Sci Res Ctr Tradit Chinese Med, Nanning 530200, Peoples R China;[5]East China Univ Sci & Technol, Sch Chem & Mol Engn, Shanghai 200237, Peoples R China

年份：2021

卷号：164

起止页码：13

外文期刊名：FREE RADICAL BIOLOGY AND MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000621339700002)】；

基金：This work was supported by the National Natural Science Foundation of China (Nos. 21822805, 22078098, 81973300 and 21908065), China Post-doctoral Science Foundation (No. 2019M651427, 2020T130197), the Commission of Science and Technology of Shanghai Municipality (18430711000).

语种：英文

外文关键词：Nitric oxide; N-nitrosated dye; Reduction-triggered release; Fluorescence; Ischemia-reperfusion protection

摘要：Nitric oxide donors (NODs) are indispensable in biological research and disease treatment. NODs had been utilized to treat cardiovascular diseases in clinic and many others are under trial. Thiols are typically required for these donors to release NO. Yet, their mechanism is complex and often lead to resistance. Herein, we reported that N-nitrosated electron-deficient dyes are capable of NO release with one-electron reduction. A fluomphore is generated simultaneously, whose fluorescence is harnessed to monitor the profile of NO release. Through electrochemical and spectral studies, NOD f3 was found to exhibit good biocompatibility and high reduction efficiency and its potentials in cell-protection in oxygen and glucose deprivation (OGD) models were showcased with endothelial cells. This work aims at offering a new approach to design reduction-triggered NOD, which have therapeutic potentials in ischemia-reperfusion.