二十二碳六烯酸乙酯对沙土鼠缺血再灌注脑损伤及水肿作用的研究(英文)

Protective Effects of Ethyl Docosahexaenoate on Reperfusion Injury and Brain Edema Following Transient Cerebral Ischemia in Gerbils

研究二十二碳六烯酸乙酯(E-DHA)对沙土鼠缺血再灌注脑损伤及其脑水肿的影响。选用雄性断奶沙土鼠灌胃给予二十二碳六烯酸乙酯(150 mg/kg·d))或等体积溶媒 10周,阻断沙土鼠双侧颈总动脉血流 10 min,造成缺血再灌注模型;测定再灌注后脑组织中丙二醛(MDA)水平,还原型谷胱甘肽(GSH)含量,超歧化氧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和钾、钠-ATP酶(Na^+,K^+-ATPase)活性,脑水含 量,钠、钾离子浓度及海马CA1区神经细胞存活百分数。结果表明:E-DHA预处理显著降低缺血再灌注沙土鼠脑组织MDA水平,阻止GSH含量、GSH-PX和Na^+,K^+-ATPase活性下降,而对SOD的活性未表现出明显作用;E-DHA亦调节缺血再灌注沙土鼠脑组织钠、钾离子浓度,减轻缺血再灌注所致的脑水肿和神经细胞死亡。提示E-DHA对脑缺血再灌注脑损伤有显著保护作用,机制可能其与抗氧化作用有关。

The protective effects of ethyl docosahexaenoate(E-DHA)on cerebral injury and brain edema induced to transient cerebral ischemia/reperfusion were investigated in gerbils. Weanling male gerbils were orally pretreated with either E-DHA( 150 mg/(kg·d))or vehicle for 10 weeks and subjected to bilateral occlusion of common carotid arteries for 10 minutes. The superoxide dismutase (SOD)activity was not modified significantly. However, the pretreatment with E-DHA significantly reduced postischemic brain malonildialdehyde(MDA)levels, and protected the reduced glutathione (GSH) contents from depletion and the activities of glutathione peroxidase (GSH-PX) and Na~ + - and K^+-ATPase from decline. In addition, the pretreatment with E-DHA significantly reduced postischemic brain edema by modulating the sodium and potassium ion concentrations. The delayed neuronal death in the CA1 of the hippocampus was significantly attenuated in E-DHA treated animals. These results suggested that the neuroprotective effects of E-DHA in gerbil cerebral ischemia/ reperfusion might be due to its antioxidant property.