文献类型：期刊文献

英文题名：A hypoxia-activated near infrared fluorescent probe for cyclooxygenase-2 and in vivo imaging for tumor and inflammation

作者：Ti, Yuezheng[1]; Yu, Ling[2]; Tang, Yao[1]; Jin, Tongxia[1]; Yang, Ming[1]; Wang, Rui[2]; Xu, Yufang[1]; Zhu, Weiping[1]

机构：[1] State Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of Chemical Biology, School of Pharmacy, East China University of Science and Technology, 130 Meilong Road, Shanghai, 200237, China; [2] Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, 130 Meilong Road, Shanghai, 200237, China

年份：2018

卷号：265

起止页码：582

外文期刊名：Sensors and Actuators, B: Chemical

收录：EI(收录号：20181204934331)

语种：英文

外文关键词：Infrared devices - Diagnosis - Fluorophores - Lanthanum compounds - Fluorescence spectroscopy - Pathology - Probes

摘要：Tumor is one of the most serious diseases, and its early diagnosis is of great significance for improving the prognosis and patient survival rate. Herein, aiming at the detection of cyclooxygenase-2 (COX-2), which plays an important role in tumorigenesis, we synthesized a NIR fluorescent probe YZP1, by using near infrared fluorescent dye Cy5.5 as the fluorophore and indomethacin (IMC) as the targeting group. Due to the quenching effect of azo group, the fluorescence of YZP1 was quenched. Under hypoxia condition and the reduction of Cytochrome P450 reductase, the azo bond of YZP1 was broken, and the fluorescence quantum yield increased from 0.0028 to 0.125. Furthermore, when HeLa cells were co-incubated with YZP1 under hypoxia condition, remarkable red fluorescence were observed, and the ratio of fluorescence intensity between hypoxic and normoxic cells could reach 9 folds. After treated with the celecoxib, an inhibitor of COX-2, of different concentrations, the fluorescence will be weakened gradually, which verify the binding of YZP1 and COX-2. Finally, by using mouse inflammation model and tumor xenograft model, the in vivo imaging ability of YZP1 was also demonstrated. ? 2018 Elsevier B.V.