中文摘要：

本实验旨在观察去甲二氢愈创木酸（nordihydroguaiaretic acid,NDGA）对大鼠局灶性脑缺血后炎症细胞聚集的作用及其机制。在大鼠大脑中动脉阻塞30min后进行再灌注72h,在再灌注30min,2、24、48h时分别腹腔注射一次NDGA（5、10mg/kg）。再灌注72h后检测脑损伤、内源性IgG渗出、中性粒细胞和巨噬细胞/小胶质细胞聚集、细胞间黏附分子-1（intercellular adhesion molecule-1,ICAM-1）mRNA和蛋白表达,并在再灌注3h后检测脑内5-脂氧酶（5-lipoxygenase,5-LOX）的催化产物白三烯B4（leukotriene B4,LTB4）和半胱氨酰白三烯（cysteinyl leukotrienes,CysLTs）含量。结果显示：NDGA能显著改善脑损伤,减少内源性IgG渗出、中性粒细胞浸润、ICAM-1mRNA和蛋白表达,同时降低脑内LTB4和CysLTs含量,但对巨噬细胞/小胶质细胞聚集没有影响。上述结果提示,NDGA对脑缺血亚急性期炎症反应的抑制主要表现为减少中性粒细胞浸润,机制可能与抑制5-LOX激活有关。

英文摘要：

The aim of the present study is to investigate the role of nordihydroguaiaretic acid （NDGA） on inflammatory cells accumu- lation after focal cerebral ischemia and the underlying mechanism.Focal cerebral ischemia was induced by 30 min of middle cerebral artery occlusion （MCAO） followed by 72 h of reperfusion.NDGA （5 and 10 mg/kg） was administered intraperitoneally 30 min,2,24,48 h after reperfusion,respectively.The brain injuries were observed by neurological and histological examination.Endogenous IgG exudation,neutrophils and macrophages/microglia accumulation,and intercellular adhesion molecule-1 （ICAM-1） protein expression were determined by immunohistochemistry 72 h after reperfusion.ICAM-1 mRNA was determined by RT-PCR 72 h after reperfusion.The catalysates of 5-lipoxygenase （5-LOX）,leukotriene B4 （LTB4） and cysteinyl leukotrienes （CysLTs）,were evaluated by ELISA 3 h after reperfusion.The results showed that NDGA ameliorated neurological dysfunction,decreased infarct volume,and inhibited endogenous IgG exudation,neutrophils infiltration,ICAM-1 mRNA and protein expression 72 h after reperfusion.Moreover,NDGA reduced the levels of LTB4 and CysLTs 3 h after reperfusion.However,NDGA did not reduce the accumulation of macrophages/ microglia 72 h after reperfusion.These results suggest that NDGA decreases neutrophil infiltration in the subacute phase of focal cerebral ischemia via inhibiting 5-LOX activation.