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一种基于近红外光驱动的上转换/碳氮/钴磷光催化剂,用于通过抑制电子-空穴对复合来高效产氢,用于阿尔茨海默病治疗。

An NIR-Driven Upconversion/CN/CoP Photocatalyst for Efficient Hydrogen Production by Inhibiting Electron-Hole Pair Recombination for Alzheimer's Disease Therapy.

机构信息

Jiangsu Key Laboratory of Brain Disease and Bioinformation, School of Pharmacy, Xuzhou Medical University, Xuzhou 221004, Jiangsu, China.

Department of Thyroid and Breast Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221004, China.

出版信息

ACS Nano. 2023 Feb 14;17(3):2222-2234. doi: 10.1021/acsnano.2c08499. Epub 2023 Jan 23.

DOI:10.1021/acsnano.2c08499
PMID:36688477
Abstract

Redox imbalance and abnormal amyloid protein (Aβ) buildup are key factors in the etiology of Alzheimer's disease (AD). As an antioxidant, the hydrogen molecule (H) has the potential to cure AD by specifically scavenging highly harmful reactive oxygen species (ROS) such as OH. However, due to the low solubility of H (1.6 ppm), the traditional H administration pathway cannot easily achieve long-term and effective accumulation of H in the foci. Therefore, how to achieve the continuous release of H is the key to improve the therapeutic effect on AD. As a corollary, we designed a rare earth ion doped g-CN upconversion photocatalyst, which can respond to NIR and realize the continuous production of H by photocatalytic decomposition of HO in biological tissue, which avoids the problem of the poor penetration of visible light. The introduction of CoP cocatalyst accelerates the separation and transfer of photogenerated electrons in g-CN, thus improving the photocatalytic activity of hydrogen evolution reaction. The morphology of the composite photocatalyst was shown by transmission electron microscopy, and the crystal structure was studied by X-ray diffractometry and Raman analysis. In addition, the ability of g-CN to chelate metal ions and the photothermal properties of CoP can inhibit Aβ and reduce the deposition of Aβ in the brain. Efficient hydrogen production therapy combined with multitarget synergism solves the problem of a poor therapeutic effect of a single target. studies have shown that UCNP@CoP@g-CN can reduce Aβ deposition, improve memory impairment, and reduce neuroinflammation in AD mice.

摘要

氧化还原失衡和异常淀粉样蛋白(Aβ)堆积是阿尔茨海默病(AD)发病机制的关键因素。作为一种抗氧化剂,氢分子(H)通过特异性清除高度有害的活性氧(ROS)如 OH,具有治疗 AD 的潜力。然而,由于 H 的低溶解度(1.6ppm),传统的 H 给药途径难以使 H 在病灶中实现长期有效的积累。因此,如何实现 H 的持续释放是提高 AD 治疗效果的关键。因此,我们设计了一种稀土离子掺杂的 g-CN 上转换光催化剂,它可以响应近红外光,并通过生物组织中 HO 的光催化分解实现 H 的连续产生,从而避免了可见光穿透性差的问题。CoP 共催化剂的引入加速了 g-CN 中光生电子的分离和转移,从而提高了光解水制氢反应的催化活性。复合光催化剂的形貌通过透射电子显微镜显示,晶体结构通过 X 射线衍射和拉曼分析进行研究。此外,g-CN 螯合金属离子的能力和 CoP 的光热特性可以抑制 Aβ并减少 Aβ在大脑中的沉积。高效的氢气生成治疗与多靶点协同作用解决了单一靶点治疗效果差的问题。研究表明,UCNP@CoP@g-CN 可以减少 Aβ的沉积,改善 AD 小鼠的记忆障碍,并减轻神经炎症。

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