title: Chronic administration of ethyl docosahexaenoate reduces gerbil brain eicosanoid productions following ischemia and reperfusion.
abstract: Arachidonic acid (AA) and its vasoactive metabolites have been implicated in the pathogenesis of brain damage induced by cerebral ischemia. The membrane AA concentrations can be reduced by changes in dietary fatty acid intake. The purpose of the present study was to investigate the effects of chronic ethyl docosahexaenoate (E-DHA) administration on the generation of eicosanoids of AA metabolism during the period of reperfusion after ischemia in gerbils. Weanling male gerbils were orally pretreated with either E-DHA (100, 200 mg/kg) or vehicle, once a day, for 10 weeks, and subjected to transient forebrain ischemia by bilateral common carotid occlusion for 10 min. E-DHA (200 mg/kg) pretreatment significantly decreased the content of brain lipid AA at the termination of treatment, prevented postischemic impaired regional cerebral blood flow (rCBF) and reduced the levels of brain prostaglandin (PG) PGF(2alpha) and 6-keto-PGF(1alpha), and thromboxane B(2) (TXB(2)), as well as leukotriene (LT) LTB(4) and LTC(4) at 30 and 60 min of reperfusion compared with the vehicle, which was well associated with the attenuated cerebral edema in the E-DHA-treated brain after 48 h of reperfusion. These data suggest that the E-DHA (200 mg/kg) pretreatment reduces the postischemic eicosanoid productions, which may be due to its reduction of the brain lipid AA content.
authors.affiliation: Department of Biology, School of Life Sciences, Nanjing University, PR China.
authors.forename: Dehua
authors.initials: D
authors.lastname: Cao
authors.forename: Chen
authors.initials: C
authors.lastname: Zhou
authors.forename: Liping
authors.initials: L
authors.lastname: Sun
authors.forename: Renhao
authors.initials: R
authors.lastname: Xue
authors.forename: Jun
authors.initials: J
authors.lastname: Xu
authors.forename: Zhili
authors.initials: Z
authors.lastname: Liu
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D016718:Arachidonic Acid / Q000032:analysis; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D001923:Brain Chemistry; D001929:Brain Edema; D002545:Brain Ischemia / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D015237:Dinoprost / Q000032:analysis; D004281:Docosahexaenoic Acids / Q000008:administration & dosage* / Q000032:analysis; D015777:Eicosanoids / Q000096:biosynthesis*; D005227:Fatty Acids / Q000032:analysis; D005849:Gerbillinae; D007975:Leukotriene B4 / Q000032:analysis; D017997:Leukotriene C4 / Q000032:analysis; D008055:Lipids / Q000032:analysis; D008297:Male; D015424:Reperfusion; D013929:Thromboxane B2 / Q000032:analysis
chemical_list: D015777:Eicosanoids; D005227:Fatty Acids; D008055:Lipids; D007975:Leukotriene B4; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D017997:Leukotriene C4; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost