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Discovery of a NADPH oxidase inhibitor, (E)-3-cyclohexyl-5-(4-((2-hydroxyethyl)(methyl)amino)benzylidene)-1-methyl-2-thioxoimidazolidin-4-oneone, as a novel therapeutic for Parkinson's disease

Title
Discovery of a NADPH oxidase inhibitor, (E)-3-cyclohexyl-5-(4-((2-hydroxyethyl)(methyl)amino)benzylidene)-1-methyl-2-thioxoimidazolidin-4-oneone, as a novel therapeutic for Parkinson's disease
Authors
Shim S.Jeong D.U.Kim H.Kim C.Y.Park H.Jin Y.Kim K.M.Lee H.J.Kim D.H.Bae Y.S.Choi Y.
Ewha Authors
배윤수이화정
SCOPUS Author ID
배윤수scopus; 이화정scopus
Issue Date
2022
Journal Title
European Journal of Medicinal Chemistry
ISSN
0223-5234JCR Link
Citation
European Journal of Medicinal Chemistry vol. 244
Keywords
Blood-brain barrier (BBB) permeabilityMPTP-Induced PD mouse ModelNADPH Oxidase (Nox)Nox inhibitorParkinson's diseaseReactive oxygen species (ROS)
Publisher
Elsevier Masson s.r.l.
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Several lines of evidence indicated that generation of NADPH oxidase (Nox)-mediated reactive oxygen species are associated with neuronal inflammation, leading to Parkinson's disease (PD). Novel benzylidene-1-methyl-2-thioxoimidazolidin-one derivatives as Nox inhibitors were designed and synthesized in order to increase blood-brain barrier (BBB) permeability to target Nox in brain cells. In lucigenin chemiluminescence assay, eight compounds showed excellent inhibition activity against NADPH oxidases and parallel artificial membrane permeability assay (PAMPA) identified compound 11 with high passive permeability. To validate the effect of compound 11 on neuronal inflammation, we tested the regulatory activity of compound 11 in lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines in BV-2 microglial cells and LPS-mediated microglial migration. Treatment of BV2 cells with compound 11 resulted in suppressed production of pro-inflammatory cytokines and migration activity of BV2 cells in response to LPS. To evaluate the therapeutic efficacy of compound 11 in PD animal model, compound 11 was applied to MPTP-induced PD mouse model. Oral administration of compound 11 (30 mg/kg/daily, 4 weeks) into the mice resulted in suppression of dopaminergic neuronal death in substantia nigra (SN) and in striatum as well as inhibition of microglial migration into SN. These results implicate compound 11 as a novel therapeutic agent for the treatment of PD. © 2022 Elsevier Masson SAS
DOI
10.1016/j.ejmech.2022.114854
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자연과학대학 > 생명과학전공 > Journal papers
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