Please use this identifier to cite or link to this item:
|Title:||A New Generation of Arachidonic Acid Analogues as Potential Neurological Agent Targeting Cytosolic Phospholipase A2||Authors:||Ng C.Y.
|Issue Date:||2017||Citation:||Ng 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||Abstract:||Cytosolic 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).||Source Title:||Scientific Reports||URI:||https://scholarbank.nus.edu.sg/handle/10635/175164||ISSN:||20452322||DOI:||10.1038/s41598-017-13996-8|
|Appears in Collections:||Elements|
Show full item record
Files in This Item:
|10_1038_s41598-017-13996-8.pdf||3.49 MB||Adobe PDF|
checked on Apr 22, 2021
checked on Apr 16, 2021
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.