固态电子介导的Z-Scheme异质结构的半导体纳米材料诱导双重编程细胞死亡进行黑色素瘤治疗
Solid-state electron-mediated z-scheme heterostructured semiconductor nanomaterials induce dual programmed cell death for melanoma therapy
影响因子:12.60000
分区:生物学1区 Top / 生物工程与应用微生物1区 纳米科技2区
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
摘要
程序性细胞死亡（PCD）途径在功能上无关紧要，容易感染或潜在的肿瘤细胞，强调其在维持内部环境稳定性并阻止癌症和许多其他疾病方面的重要作用。 PCD包括各种形式，例如凋亡，铜死亡，铁死亡和细胞凋亡。然而，新兴的固态电子介导的Z-Scheme异质结构的半导体纳米材料具有高电子孔（E-H+）分离，作为一种诱导PCD的新方法。我们合成BI2S3-BI2O3-AU-PEG纳米棒（BB-A-PNRS）Z-Scheme异质结构半导体具有较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，该光通过提供氧（O2）并通过E-H+转移将其转换为氧（1O2）的单线性状态来模仿过氧化氢酶的作用。其次，它们与肿瘤中的过氧化氢（H2O2）和水（H2O）反应，产生羟基自由基（•OH），诱导凋亡。有趣的是，caspase-1/Gasdermin D（GSDMD）依赖性的常规流动性途径诱导的细胞凋亡被凋亡和活性氧（ROS）激活，这会导致损伤相关的分子模式（DAMP）的强烈释放，导致炎症性死亡，导致炎症性死亡。反过来，这激活了免疫学环境以实现免疫原性死亡（ICD）。 BB-A-P可以实现计算机断层扫描成像，从而可以看到治疗。 BB-A-P激活的双PCD可以看作是一种有效的细胞死亡方式，可以协调细胞内环境，并且各种途径相互关联并相互加强，这显示出有希望的治疗作用，并提供了消除缺氧肿瘤的新策略。
Abstract
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.