Binyang Du

Prof. Binyang Du

Department of Polymer Science and Engineering, Zhejiang University, Yuquan Campus, Polymer Building, Room 419, Zheda Road No. 38, Hangzhou 310027, China
orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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8 June 2020 in Particle and Fibre Toxicology
Verified
Journal Article
Open access
PDF file
MWMingxiang Wang
Mingxiang Wang
JLJin Li
Jin Li
SDShunni Dong
Shunni Dong
XCXiaobo Cai
Xiaobo Cai
Aili SimaitiAili Simaiti
Aili Simaiti
WYWei Yang
Wei Yang
Background: Wide applications of nanoparticles (NPs) have raised increasing concerns about safety to humans. Oxidative stress and inflammation are extensively investigated as mechanisms for NPs-induced toxicity. Autophagy and lysosomal dysfunction are emerging molecular mechanisms. Inhalation is one of the main pathways of exposing humans to NPs, which has been reported to induce severe pulmonary inflammation. However, the underlying mechanisms and, more specifically, the interplays of above-mentioned mechanisms in NPs-induced pulmonary inflammation are still largely obscure. Considered that NPs exposure in modern society is often unavoidable, it is highly desirable to develop effective strategies that could help to prevent nanomaterials-induced pulmonary inflammation. Results: Pulmonary inflammation induced by intratracheal instillation of silica nanoparticles (SiNPs) in C57BL/6 mice was prevented by PJ34, a poly (ADP-ribose) polymerase (PARP) inhibitor. In human lung bronchial epithelial (BEAS-2B) cells, exposure to SiNPs reduced cell viability, and induced ROS generation, impairment in lysosome function and autophagic flux. Inhibition of ROS generation, PARP and TRPM2 channel suppressed SiNPs-induced lysosome impairment and autophagy dysfunction and consequent inflammatory responses. Consistently, SiNPs-induced pulmonary inflammation was prevented in TRPM2 deficient mice. Conclusion: The ROS/PARP/TRPM2 signaling is critical in SiNPs-induced pulmonary inflammation, providing novel mechanistic insights into NPs-induced lung injury. Our study identifies TRPM2 channel as a new target for the development of preventive and therapeutic strategies to mitigate nanomaterials-induced lung inflammation. Graphical

9 January 2019 in ACS Applied Materials & Interfaces
Verified
Journal Article
Closed access
YLYongzhi Liang
Yongzhi Liang
JXJinqiao Xue
Jinqiao Xue
Binyang DuBinyang Du
Binyang Du
JNJingjing Nie
Jingjing Nie

7 June 2017 in ACS Applied Materials & Interfaces
Verified
Journal Article
Closed access
XZXianjing Zhou
Xianjing Zhou
JNJingjing Nie
Jingjing Nie
Binyang DuBinyang Du
Binyang Du

3 March 2017 in Macromolecules
Verified
Journal Article
Closed access
BFBin Fan
Bin Fan
RWRui-Yang Wang
Rui-Yang Wang
XWXiang-Yue Wang
Xiang-Yue Wang
JXJunting Xu
Junting Xu
Binyang DuBinyang Du
Binyang Du
ZFZhi-Qiang Fan
Zhi-Qiang Fan

27 April 2017 in Journal of Materials Chemistry C
Verified
Journal Article
Closed access
PDF file
Bin LiuBin Liu
Bin Liu
YWYa-Ling Wang
Ya-Ling Wang
WBWei Bai
Wei Bai
JXJunting Xu
Junting Xu
ZXZhi-Kang Xu
Zhi-Kang Xu
Binyang DuBinyang Du
Binyang Du
The fluorescent properties of a linear poly(hydroxyurethane) (P1) from carbon dioxide, siloxane (Si–O–Si)-containing bisepoxide and diamine are described. P1 showed strong photoluminescence with a quantum yield of up to 23.6%, high photostability, and broad absorption and emission spectra either in bulk or solution. The flexibility and hydrophobicity of the Si–O–Si linkage in P1 were utilized to drive the intense aggregation of hydroxyurethane chromophores which combined with the hydrogen bonding interactions lead to strong photoluminescence. P1 was used as a single phosphor film for fabricating a low voltage, cool white light-emitting diode device with competitive performances.

13 March 2014 in ACS Applied Materials & Interfaces
Verified
Journal Article
Closed access
XZXianjing Zhou
Xianjing Zhou
YZYuanyuan Zhou
Yuanyuan Zhou
JNJingjing Nie
Jingjing Nie
ZJZhichao Ji
Zhichao Ji
JXJunting Xu
Junting Xu
Binyang DuBinyang Du
Binyang Du