光热治疗
纳米颗粒
活性氧
单体
化学
辐照
铜
生物物理学
纳米技术
体内
材料科学
生物化学
有机化学
聚合物
生物技术
物理
生物
核物理学
作者
Hongyu Zhang,Changlong Hao,Aihua Qu,Maozhong Sun,Liguang Xu,Chuanlai Xu,Hua Kuang
标识
DOI:10.1002/anie.202002028
摘要
Abstract The accumulation and deposition of β‐amyloid (Aβ) plaques in the brain is considered a potential pathogenic mechanism underlying Alzheimer's disease (AD). Chiral l/d ‐Fe x Cu y Se nanoparticles (NPs) were fabricated that interfer with the self‐assembly of Aβ42 monomers and trigger the Aβ42 fibrils in dense structures to become looser monomers under 808 nm near‐infrared (NIR) illumination. d ‐Fe x Cu y Se NPs have a much higher affinity for Aβ42 fibrils than l ‐Fe x Cu y Se NPs and chiral Cu 2− x Se NPs. The chiral Fe x Cu y Se NPs also generate more reactive oxygen species (ROS) than chiral Cu 2− x Se NPs under NIR‐light irradiation. In living MN9D cells, d ‐NPs attenuate the adhesion of Aβ42 to membranes and neuron loss after NIR treatment within 10 min without the photothermal effect. In‐vivo experiments showed that d ‐Fe x Cu y Se NPs provide an efficient protection against neuronal damage induced by the deposition of Aβ42 and alleviate symptoms in a mouse model of AD, leading to the recovery of cognitive competence.
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