光动力疗法
迷迭香酸
活性氧
免疫原性细胞死亡
肿瘤微环境
癌症研究
化学
转移
光热治疗
生物物理学
程序性细胞死亡
抗氧化剂
癌症
生物化学
材料科学
细胞凋亡
纳米技术
医学
生物
有机化学
内科学
肿瘤细胞
作者
Yang Zhou,Yiwei Zhang,Chaoqing Jiang,Yuxiu Chen,Fan Tong,Jing Wang,Yazhen Wang,Xue Xia,Huile Gao
出处
期刊:Small
[Wiley]
日期:2023-02-08
卷期号:19 (23)
被引量:19
标识
DOI:10.1002/smll.202300594
摘要
A primary concern about photodynamic therapy (PDT) is its inability to regulate the generation levels of reactive oxidative species (ROS) based on the complex microenvironment, resulting in the impairment toward normal tissues and immunosuppression. Besides, tumor metastasis also compromises PDT's efficacy and drives mortality. However, it is very challenging to achieve such two goals within one nanosystem. Here, the nanoassembly (CPR) with self-regulated photodynamic and antimetastasis properties comprises three parts: chlorin e6-conjugated β-cyclodextrin (CD-Ce6) acts as the main PDT agent and ferrocene (Fc)-terminated phenylboronic acid-containing conjugates entering into the cavity of CD-Ce6, as well as rosmarinic acid (RA)-boronic acid crosslinked shell. Compared with non-crosslinked counterpart, CPR displays better stability and enhanced tumor accumulation. Under laser irradiation, CPR generates plenty of ROS to damage tumor cells and induce immunogenic cell death. Mildly acidic TME partly cleaves the crosslinkers to dissociate antioxidant RAs from micelles, which together with Fc in CPR scavenge PDT-induced ROS in the TME. By contrast, under acidic lysosomal conditions, Fc catalyzes abundant H2 O2 in tumor cells to produce highly cytotoxic •OH, while RA continuously reduces ferroptosis-generated Fc+ into Fc, both to augment the PDT efficacy in tumor cells. CPR also remarkably hinders the epithelial-mesenchymal transition to prevent the lung metastasis.
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