Prior, Allan M.Zhang, ManBlakeman, NinaDatta, PalikaPham, HungChen, QianYoung, Lindon H.Weis, Margaret T.Hua, Duy H.2014-05-302014-05-302014-02-15http://hdl.handle.net/2097/17802Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were examined. Two methods, a cell-based assay of ACSL activity and an in situ [¹⁴C]-palmitate incorporation into extractable lipids were used to study the inhibition. Using an in vivo leukocyte recruitment inhibition protocol, the translocation of one or more cell adhesion molecules from the cytoplasm to the plasma membrane on either the endothelium or leukocyte or both was inhibited by inhibitors 1, 9, and triacsin C. The results suggest that inhibition of ACSL may attenuate the vascular inflammatory component associated with ischemia reperfusion injury and lead to a decrease of infarct expansion.en-USThis Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).HydroxytriazeneIschemia reperfusion injuryLong chain fatty acyl-CoA synthetase (ACSL)InhibitorsOxadiazolidine dioneTriacsin CArticle (author version)