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拓扑结构调控纳米催化剂用于铁死亡介导的癌症光疗。

Topology-regulated nanocatalysts for ferroptosis-mediated cancer phototherapy.

机构信息

Department of Anesthesiology, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200030, China; School of Materials and Chemistry, Institute of Bismuth, Shanghai Collaborative Innovation Center of Energy Therapy for Tumors, University of Shanghai for Science and Technology, Shanghai 200093, China.

School of Materials and Chemistry, Institute of Bismuth, Shanghai Collaborative Innovation Center of Energy Therapy for Tumors, University of Shanghai for Science and Technology, Shanghai 200093, China.

出版信息

J Colloid Interface Sci. 2024 Feb 15;656:320-331. doi: 10.1016/j.jcis.2023.11.119. Epub 2023 Nov 20.

Abstract

Ferroptosis-mediated tumor treatment is constrained by the absence of single-component, activatable multifunctional inducers. Given this, a topological synthesis strategy is employed to develop an efficient bismuth-based semiconductor nano-photocatalyst (BiO:S) for tumor ferroptosis therapy. Photo-excited electrons can participate in the reduction reaction to produce harmful reactive oxygen species (ROS) when exposed to near-infrared light. Meanwhile, photo-excited holes can contribute to the oxidation reaction to utilize extra glutathione (GSH) in tumors. In the acidic tumor microenvironment, bismuth ions generated from BiO:S may further cooperate with GSH to amplify oxidative stress damage and achieve biodegradation. Both promote ferroptosis by downregulating glutathione peroxidase 4 (GPX4) expression. Besides, sulfur doping optimizes its near-infrared light-induced photothermal conversion efficiency, benefiting its therapeutic effect. Thus, bismuth ions and holes synergistically drive photo-activable ferroptosis in this nanoplatform, opening up new avenues for tumor therapy.

摘要

铁死亡介导的肿瘤治疗受到缺乏单一成分、可激活多功能诱导剂的限制。有鉴于此,采用拓扑合成策略开发了一种高效的基于铋的半导体纳米光催化剂(BiO:S),用于肿瘤铁死亡治疗。当暴露于近红外光时,光激发电子可以参与还原反应以产生有害的活性氧(ROS)。同时,光激发空穴可以有助于氧化反应以利用肿瘤中的额外谷胱甘肽(GSH)。在酸性肿瘤微环境中,BiO:S 产生的铋离子可能进一步与 GSH 合作,放大氧化应激损伤并实现生物降解。两者都通过下调谷胱甘肽过氧化物酶 4(GPX4)的表达来促进铁死亡。此外,硫掺杂优化了其近红外光诱导的光热转换效率,有利于其治疗效果。因此,铋离子和空穴协同驱动该纳米平台中的光激活铁死亡,为肿瘤治疗开辟了新途径。

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