论文部分内容阅读
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。
This experiment aimed to observe the effect of nordihydroguaiaretic acid (NDGA) on the aggregation of inflammatory cells after focal cerebral ischemia in rats and its mechanism. Rats in the middle cerebral artery occluded for 30 min were reperfused for 72 h. NDGA (5, 10 mg / kg) was intraperitoneally injected at 30 min, 2, 24, 48 h after reperfusion. After 72h of reperfusion, brain injury, exudation of endogenous IgG, aggregation of neutrophils and macrophages / microglia, ICAM-1 mRNA and protein , And the catalytic products of 5-lipoxygenase (5-LOX), leukotriene B4 (LTB4) and cysteinyl leukotrienes CysLTs) content. The results showed that: NDGA can significantly improve brain injury, reduce endogenous IgG exudation, neutrophil infiltration, ICAM-1mRNA and protein expression, while reducing brain content of LTB4 and CysLTs, but macrophages / microglia Aggregation has no effect. The above results suggest that, NDGA inhibition of subacute inflammatory response to cerebral ischemia mainly for the reduction of neutrophil infiltration, the mechanism may be related to the inhibition of 5-LOX activation.