目的：观察二氢杨梅素（ dihydromyricetin ，DMY）对小鼠局灶性脑缺血再灌注（ ischemia／reperfusion ， I／R）损伤后炎症反应的影响。方法雄性昆明种小鼠随机分为3组，即假手术组、I／R模型组及DMY（500 mg／kg）组。改良线栓法制备小鼠大脑中动脉阻塞／再灌注（ middle cerebral artery occlusion ／reperfusion，MCAO／R）局灶性脑缺血（3 h）再灌注（24 h）损伤模型。术前10 d开始灌胃给药，每天1次，并在缺血前1 h及再灌注后12 h各给药1次。再灌注24 h后取脑，免疫组织化学检测小胶质细胞标记物离子钙接头蛋白（ ionized calcium binding adaptor molecule-1，Iba1）和5-脂氧合酶（5-lipoxygenase，5-LOX）表达；ELISA法检测缺血脑组织匀浆炎症因子TNF-α和5-LOX代谢物白三烯B4（leukotrienes B4，LTB4）、半胱氨酰白三烯（cysteinyl leukotrienes，CysLTs）含量。结果与模型组比较，DMY 500 mg／kg抑制小胶质细胞活化并降低TNF-α水平，降低缺血脑组织5-LOX蛋白表达并减少LTB4与CysLTs的产生（P＜0．05或P＜0．01）。结论 DMY可减轻局灶性脑I／R损伤炎症反应，与抑制5-LOX有关。%Objective To study the influences of dihydromyricetin ( DMY) on inflammatory reaction induced by fo-cal cerebral ischemia-reperfusion ( I/R) injury in mice.Methods Male Kunming mice were randomly divided into 3 groups:sham group,I/R group and DMY 500 mg/kg group.Mice model of middle cerebral artery occlusion (MCAO,3 h)/reperfusion (24 h) model was established by the improved intraluminal filament technique .Drugs were given orally 10 d (once a day ) before the surgery ,1 h before ischemia and 12 h after reperfusion .After reperfusion for 24 h,the expressions of ionized calcium binding adaptor molecule-1( Iba1) and 5-LOX in mice brain were assessed by immunohistochemistry;the contents of TNF-αand 5-LOX metabolites ( LTB4 and CysLTs ) in ischemic brain tissue were detected by ELISA .Results Compared with the I/R group,DMY at 500 mg/kg could obviously inhibit the activation of microglia ,lower the level of TNF-α,and reduce the expression of 5-LOX and the production of LTB4 and CysLTs (P<0.05或P<0.01).Con clusion DMY reduces inflammatory reaction induced by focal cerebral I /R injury,which might be associated with its inhibition on 5-LOX.
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