Geng Huafeng, Chen Ke, Cao Lu, Liu Luntao, Huang Yue, Liu Junbao
Department of Obstetrics and Gynecology, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun 130033, China.
MOE Key Laboratory for Analytical Science of Food Safety and Biology, College of Chemistry, Fuzhou University, Fuzhou 350108, People's Republic of China.
Langmuir. 2023 Mar 21;39(11):4037-4048. doi: 10.1021/acs.langmuir.2c03399. Epub 2023 Mar 12.
By directly harming cancer cells, radiotherapy (RT) is a crucial therapeutic approach for the treatment of cancers. However, the efficacy of RT is reduced by the limited accumulation and short retention time of the radiosensitizer in the tumor. Herein, we developed hypoxia-triggered in situ aggregation of nanogapped gold nanospheres (AuNNP@PAA/NIC NPs) within the tumor, resulting in second near-infrared window (NIR-II) photoacoustic (PA) imaging and enhanced radiosensitization. AuNNP@PAA/NIC NPs demonstrated increased accumulation and retention in hypoxic tumors, mainly due to the hypoxia-triggered aggregation. After aggregation of AuNNP@PAA/NIC NPs, the absorption of the system extended from visible light to NIR-II light owing to the plasmon coupling effects between adjacent nanoparticles. Compared to the normoxic tumor, the PA intensity at 1200 nm in the hypoxic tumor increased from 0.42 to 1.88 at 24 h postintravenous injection of AuNNP@PAA/NIC NPs, leading to an increase of 4.5 times. This indicated that the hypoxic microenvironment in the tumor successfully triggered the in situ aggregation of AuNNP@PAA/NIC NPs. The in vivo radiotherapeutic effect demonstrated that this hypoxia-triggered in situ aggregation of radiosensitizers significantly enhanced radiosensitization and thus resulted in superior cancer radiotherapeutic outcomes.
放射疗法（RT）通过直接损伤癌细胞，是治疗癌症的一种关键治疗方法。然而，由于放射增敏剂在肿瘤中的积累有限且保留时间短，RT的疗效会降低。在此，我们开发了一种在肿瘤内由缺氧触发的纳米间隙金纳米球（AuNNP@PAA/NIC NPs）原位聚集，从而实现了第二近红外窗口（NIR-II）光声（PA）成像并增强了放射增敏作用。AuNNP@PAA/NIC NPs在缺氧肿瘤中表现出增加的积累和保留，这主要归因于缺氧触发的聚集。AuNNP@PAA/NIC NPs聚集后，由于相邻纳米颗粒之间的等离子体耦合效应，该系统的吸收从可见光扩展到了NIR-II光。与常氧肿瘤相比，在静脉注射AuNNP@PAA/NIC NPs后24小时，缺氧肿瘤中1200 nm处的PA强度从0.42增加到1.88，增加了4.5倍。这表明肿瘤中的缺氧微环境成功触发了AuNNP@PAA/NIC NPs的原位聚集。体内放射治疗效果表明，这种由缺氧触发的放射增敏剂原位聚集显著增强了放射增敏作用，从而产生了优异的癌症放射治疗效果。
