固态电子介导的 z 型异质结构半导体纳米材料诱导黑色素瘤治疗的双重程序性细胞死亡。
Solid-state electron-mediated z-scheme heterostructured semiconductor nanomaterials induce dual programmed cell death for melanoma therapy.
发表日期:2024 Aug 31
作者:
Yiping Ren, Yun Wang, Cheng Chen, Xiang Yan, Minghao Chao, Yuting Li, Dehong Yu, Yuqi Huang, Xiaoyang Hou, Fenglei Gao, Guan Jiang, Ming Guan
来源:
JOURNAL OF NANOBIOTECHNOLOGY
摘要:
程序性细胞死亡(PCD)途径可去除功能不重要、易感染或潜在致瘤的细胞,强调其在维持内部环境的稳定性以及预防癌症和许多其他疾病方面的重要作用。 PCD包括多种形式,例如细胞凋亡、铜死亡、铁死亡和细胞焦亡。然而,新兴的具有高电子空穴(e-h)分离度的固态电子介导Z型异质结构半导体纳米材料作为诱导PCD的新方法尚未得到充分研究。我们合成的Bi2S3-Bi2O3-Au-PEG纳米棒(BB-A-P NRs)Z型异质结构半导体具有更高的氧化还原能力和生物相容性。首先,BB-A-P NR 被近红外 (NIR) 光激发,近红外 (NIR) 光通过提供氧气 (O2) 并通过 e-h 转移将其转化为单线性氧 (1O2) 状态来模拟过氧化氢酶的作用。其次,它们与肿瘤内的过氧化氢(H2O2)和水(H2O)反应产生羟自由基(•OH),诱导细胞凋亡。有趣的是,Caspase-1/Gasdermin D (GSDMD) 依赖的传统细胞焦亡途径诱导细胞焦亡,由细胞凋亡和活性氧 (ROS) 激活,导致损伤相关分子模式 (DAMP) 的强烈释放,导致细胞的炎症性死亡。肿瘤细胞。这反过来又激活免疫环境以实现免疫原性细胞死亡(ICD)。 BB-A-P 可实现计算机断层扫描成像,从而实现治疗的可视化。 BB-A-P激活的双PCD可以被视为协调细胞内环境的有效细胞死亡模式,且各种途径相互关联、相互促进,显示出良好的治疗效果,为消除缺氧肿瘤提供了新的策略。©2024。作者。
The programmed cell death (PCD) pathway removes functionally insignificant, infection-prone, or potentially tumorigenic cells, underscoring its important role in maintaining the stability of the internal environment and warding off cancer and a host of other diseases. PCD includes various forms, such as apoptosis, copper death, iron death, and cellular pyroptosis. However, emerging solid-state electron-mediated Z-scheme heterostructured semiconductor nanomaterials with high electron-hole (e-h+) separation as a new method for inducing PCD have not been well studied. We synthesize the Bi2S3-Bi2O3-Au-PEG nanorods (BB-A-P NRs) Z-scheme heterostructured semiconductor has a higher redox capacity and biocompatibility. Firstly, the BB-A-P NRs are excited by near-infrared (NIR) light, which mimics the action of catalase by supplying oxygen (O2) and converting it to a single-linear state of oxygen (1O2) via e-h+ transfer. Secondly, they react with hydrogen peroxide (H2O2) and water (H2O) in tumor to produce hydroxyl radicals (•OH), inducing apoptosis. Intriguingly, the Caspase-1/Gasdermin D (GSDMD)-dependent conventional pyroptosis pathway induced cellular pyroptosis activated by apoptosis and reactive oxygen species (ROS) which causes the intense release of damage associated molecular patterns (DAMPs), leading to the inflammatory death of tumor cells. This, in turn, activates the immunological environment to achieve immunogenic cell death (ICD). BB-A-P enables computed tomography imaging, which allows for visualization of the treatment. BB-A-P activated dual PCD can be viewed as an effective mode of cell death that coordinates the intracellular environment, and the various pathways are interrelated and mutually reinforcing which shows promising therapeutic effects and provides a new strategy for eliminating anoxic tumors.© 2024. The Author(s).