Minocycline inhibits 5-lipoxygenase activation and brain inflammation after focal cerebral ischemia in rats
Minocycline inhibits 5-lipoxygenase activation and brain inflammation after focal cerebral ischemia in rats
复制标题
DOI：
10.1111/j.1745-7254.2007.00578.x
复制
发表时间：
2007-06-01
影响因子：
8.2
通讯作者：
Wei, Er-qing
中科院分区：
文献类型：
--
作者：
Chu, Li-sheng;Fang, San-hua;Wei, Er-qing
目的：探讨米诺环素对大鼠化学后脑损伤的抗炎作用是否通过抑制5-脂氧合酶（5-LOX）表达和酶活性介导。方法：大脑中动脉闭塞致局灶性脑缺血30min后再灌注。再灌注72 h后测定缺血损伤、内源性IgG渗出、中性粒细胞和巨噬细胞/小胶质细胞的积累以及5-LOX mRNA的表达。再灌注后3 h测定5-LOX代谢物（白三烯B-4和半胱氨酸白三烯）。结果：二甲胺四环素（22.5和45 mg/kg， ig, 3 d）在再灌注72 h后减轻了缺血损伤、IgG渗出和中性粒细胞和巨噬细胞/小胶质细胞的积累。在再灌注72 h后抑制5-LOX的表达，在再灌注3 h后抑制白三烯的产生。结论：米诺环素对脑缺血后炎症的抑制作用可能与抑制5-LOX的表达和酶的激活有关。
Aim: To determine whether the anti-inflammatory effect of minocycline on postis-chemic brain injury is mediated by the inhibition of 5-lipoxygenase (5-LOX) expression and enzymatic activation in rats. Methods: Focal cerebral ischemia was induced for 30 min with middle cerebral artery occlusion, followed by reperfusion. The ischemic injuries, endogenous IgG exudation, the accumulation of neutrophils and macrophage/microglia, and 5-LOX mRNA expression were determined 72 h after reperfusion. 5-LOX metabolites (leukotriene B-4 and cysteinyl leukotrienes) were measured 3 h after reperfusion. Results: Minocycline (22.5 and 45 mg/kg, ip, for 3 d) attenuated ischemic injuries, IgG exudation, and the accumulation of neutrophils and macrophage/microglia 72 h after reperfusion. It also inhibited 5-LOX expression 72 h after reperfusion and the production of leukotrienes 3 h after reperfusion. Conclusion: Minocycline inhibited postischemic brain inflammation, which might be partly mediated by the inhibition of 5-LOX expression and enzymatic activation.