Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-017-13996-8
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dc.titleA New Generation of Arachidonic Acid Analogues as Potential Neurological Agent Targeting Cytosolic Phospholipase A2
dc.contributor.authorNg C.Y.
dc.contributor.authorKannan S.
dc.contributor.authorChen Y.J.
dc.contributor.authorTan F.C.K.
dc.contributor.authorOng W.Y.
dc.contributor.authorGo M.L.
dc.contributor.authorVerma C.S.
dc.contributor.authorLow C.-M.
dc.contributor.authorLam Y.
dc.date.accessioned2020-09-09T04:48:01Z
dc.date.available2020-09-09T04:48:01Z
dc.date.issued2017
dc.identifier.citationNg C.Y., Kannan S., Chen Y.J., Tan F.C.K., Ong W.Y., Go M.L., Verma C.S., Low C.-M., Lam Y. (2017). A New Generation of Arachidonic Acid Analogues as Potential Neurological Agent Targeting Cytosolic Phospholipase A2. Scientific Reports 7 (1) : 13683. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-017-13996-8
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/175164
dc.description.abstractCytosolic phospholipase A2 (cPLA2) is an enzyme that releases arachidonic acid (AA) for the synthesis of eicosanoids and lysophospholipids which play critical roles in the initiation and modulation of oxidative stress and neuroinflammation. In the central nervous system, cPLA2 activation is implicated in the pathogenesis of various neurodegenerative diseases that involves neuroinflammation, thus making it an important pharmacological target. In this paper, a new class of arachidonic acid (AA) analogues was synthesized and evaluated for their ability to inhibit cPLA2. Several compounds were found to inhibit cPLA2 more strongly than arachidonyl trifluoromethyl ketone (AACOCF3), an inhibitor that is commonly used in the study of cPLA2-related neurodegenerative diseases. Subsequent experiments concluded that one of the inhibitors was found to be cPLA2-selective, non-cytotoxic, cell and brain penetrant and capable of reducing reactive oxygen species (ROS) and nitric oxide (NO) production in stimulated microglial cells. Computational studies were employed to understand how the compound interacts with cPLA2. © 2017 The Author(s).
dc.sourceUnpaywall 20200831
dc.typeArticle
dc.contributor.departmentDEPT OF CHEMISTRY
dc.contributor.departmentCHEMICAL & ENVIRONMENTAL ENGINEERING
dc.contributor.departmentDEPT OF ANAESTHESIA
dc.contributor.departmentDEPT OF PHARMACY
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.1038/s41598-017-13996-8
dc.description.sourcetitleScientific Reports
dc.description.volume7
dc.description.issue1
dc.description.page13683
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