An NIR-Driven Upconversion/C 3 N 4 /CoP Photocatalyst for Efficient Hydrogen Production by Inhibiting Electron-Hole Pair Recombination for Alzheimer's Disease Therapy

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 t...

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Veröffentlicht in:ACS nano 2023-02, Vol.17 (3), p.2222-2234
Hauptverfasser: Ge, Kezhen, Li, Zheng, Wang, Ali, Bai, Zetai, Zhang, Xing, Zheng, Xin, Liu, Zhao, Gao, Fenglei
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Sprache:eng
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Zusammenfassung: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-C N upconversion photocatalyst, which can respond to NIR and realize the continuous production of H by photocatalytic decomposition of H O 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-C N , 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-C N 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-C N can reduce Aβ deposition, improve memory impairment, and reduce neuroinflammation in AD mice.
ISSN:1936-0851
1936-086X
DOI:10.1021/acsnano.2c08499