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Bin Di

Researcher at Chinese Ministry of Education

Publications -  9
Citations -  252

Bin Di is an academic researcher from Chinese Ministry of Education. The author has contributed to research in topics: Inflammasome & Pyrin domain. The author has an hindex of 6, co-authored 9 publications receiving 88 citations. Previous affiliations of Bin Di include China Pharmaceutical University.

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The NLRP3 inflammasome and COVID-19: Activation, pathogenesis and therapeutic strategies.

TL;DR: In this article, the authors introduce the canonical NLRP3 inflammasome activation pathway and review the cellular/molecular mechanisms of NNBP3 activation by SARS-CoV-2 infection (e.g., viroporins, ion flux and the complement cascade).
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5-(3,4-Difluorophenyl)-3-(6-methylpyridin-3-yl)-1,2,4-oxadiazole (DDO-7263), a novel Nrf2 activator targeting brain tissue, protects against MPTP-induced subacute Parkinson's disease in mice by inhibiting the NLRP3 inflammasome and protects PC12 cells against oxidative stress.

TL;DR: DDO-7263 improved the behavioral abnormalities induced by MPTP in mice, significantly attenuated chemically induced dopaminergic neuron loss of tyrosine hydroxylase (TH) in the substantia nigra and striatum of the mouse brain and inhibited the secretion of inflammatory factors.
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Recent advances in the NEK7-licensed NLRP3 inflammasome activation: Mechanisms, role in diseases and related inhibitors.

TL;DR: The cellular/molecular mechanisms of the NEK7-licensed NLRP3 inflammasome activation are described and the potential inhibitors that can selectively and effectively modulate either the NEk7-NLRP3 complex itself or the related molecular/cellular events are detailed.
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3-(1H-Benzo[d]imidazol-6-yl)-5-(4-fluorophenyl)-1,2,4-oxadiazole (DDO7232), a Novel Potent Nrf2/ARE Inducer, Ameliorates DSS-Induced Murine Colitis and Protects NCM460 Cells against Oxidative Stress via ERK1/2 Phosphorylation.

TL;DR: A novel effective Nrf2 activator, DDO7232, is identified, which showed protective effects on NCM460 cells and therapeutic effects on DSS-induced colitis in mice and provided an effective therapeutic option for the treatment of UC.