Details

Autor(en) / Beteiligte

• Ge, Kezhen
• Li, Zheng
• Wang, Ali
• Bai, Zetai
• Zhang, Xing
• Zheng, Xin
• Liu, Zhao
• Gao, Fenglei

Titel

An NIR-Driven Upconversion/C3N4/CoP Photocatalyst for Efficient Hydrogen Production by Inhibiting Electron–Hole Pair Recombination for Alzheimer’s Disease Therapy

Ist Teil von

• ACS nano, 2023-02, Vol.17 (3), p.2222-2234

Ort / Verlag

American Chemical Society

Erscheinungsjahr

2023

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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 (H2) 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 H2 (1.6 ppm), the traditional H2 administration pathway cannot easily achieve long-term and effective accumulation of H2 in the foci. Therefore, how to achieve the continuous release of H2 in situ is the key to improve the therapeutic effect on AD. As a corollary, we designed a rare earth ion doped g-C3N4 upconversion photocatalyst, which can respond to NIR and realize the continuous production of H2 by photocatalytic decomposition of H2O 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-C3N4, 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-C3N4 to chelate metal ions and the photothermal properties of CoP can inhibit Aβ and reduce the deposition of Aβ in the brain. Efficient in situ hydrogen production therapy combined with multitarget synergism solves the problem of a poor therapeutic effect of a single target. In vivo studies have shown that UCNP@CoP@g-C3N4 can reduce Aβ deposition, improve memory impairment, and reduce neuroinflammation in AD mice.