Preparation of monodisperse bimetallic nanorods with gold nanorod core and silver shell and their plasmonic property and SERS efficiency

2014 ◽  
Vol 45 (6) ◽  
pp. 431-437 ◽  
Author(s):  
Xu Dong ◽  
Jianfeng Zhou ◽  
Xiaoyun Liu ◽  
Danli Lin ◽  
Liusheng Zha
Small ◽  
2016 ◽  
Vol 13 (10) ◽  
pp. 1602855 ◽  
Author(s):  
Xiumei Jiang ◽  
Liming Wang ◽  
Yinglu Ji ◽  
Jinglong Tang ◽  
Xin Tian ◽  
...  

2018 ◽  
Vol 14 (11) ◽  
pp. 1953-1964 ◽  
Author(s):  
Dan Wang ◽  
Mo Dan ◽  
Yinglu Ji ◽  
Xiaochun Wu ◽  
Liming Xu ◽  
...  

2020 ◽  
Vol 21 (2) ◽  
pp. 384 ◽  
Author(s):  
Haiyun Li ◽  
Tao Wen ◽  
Tao Wang ◽  
Yinglu Ji ◽  
Yaoyi Shen ◽  
...  

With the increasing applications of silver nanoparticles (Ag NPs), the concerns of widespread human exposure as well as subsequent health risks have been continuously growing. The acute and chronic toxicities of Ag NPs in cellular tests and animal tests have been widely investigated. Accumulating evidence shows that Ag NPs can induce inflammation, yet the overall mechanism is incomplete. Herein, using gold nanorod core/silver shell nanostructures (Au@Ag NRs) as a model system, we studied the influence on mice liver and lungs from the viewpoint of metabolism. In agreement with previous studies, Au@Ag NRs’ intravenous exposure caused inflammatory reaction, accompanying with metabolic alterations, including energy metabolism, membrane/choline metabolism, redox metabolism, and purine metabolism, the disturbances of which contribute to inflammation. At the same time, dopamine metabolism in liver was also changed. This is the first time to observe the production of dopamine in non-neural tissue after treatment with Ag NPs. As the upregulation of dopamine resists inflammation, it indicates the activation of antioxidant defense systems against oxidative stress induced by Au@Ag NRs. In the end, our findings deepened the understanding of molecular mechanisms of Ag NPs-induced inflammation and provide assistance in the rational design of their biomedical applications.


2020 ◽  
Author(s):  
Dan Wang ◽  
Mo Dan ◽  
Yinglu Ji ◽  
Xiaochun Wu ◽  
Xue Wang ◽  
...  

Abstract To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4 - 20 µg.mL-1 Au@Ag NR were investigated by comet assay, γ-H2AX assay, and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells, and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release as well as the potential genotoxicity of AgNPs.


Nanoscale ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 6429-6437 ◽  
Author(s):  
Haiyun Li ◽  
Jiaqi Chen ◽  
Huizhen Fan ◽  
Rui Cai ◽  
Xinshuang Gao ◽  
...  

At sub-lethal doses, Au@Ag NRs induce oxidative stress that activates the protective autophagy of human hepatocytes.


2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Dan Wang ◽  
Mo Dan ◽  
Yinglu Ji ◽  
Xiaochun Wu ◽  
Xue Wang ◽  
...  

AbstractTo understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4–20 µg mL−1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release and the potential genotoxicity of AgNPs.


Sign in / Sign up

Export Citation Format

Share Document