Chu Li-Sheng, Fang San-Hua, Zhou Yu, Yu Guo-Liang, Wang Meng-Ling, Zhang Wei-Ping, Wei Er-Qing
Department of Pharmacology, School of Medicine, Zhejiang University, Hangzhou 310058, China.
Acta Pharmacol Sin. 2007 Jun;28(6):763-72. doi: 10.1111/j.1745-7254.2007.00578.x.
To determine whether the anti-inflammatory effect of minocycline on postischemic brain injury is mediated by the inhibition of 5-lipoxygenase (5-LOX) expression and enzymatic activation in rats.
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 B4 and cysteinyl leukotrienes) were measured 3 h after reperfusion.
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.
Minocycline inhibited postischemic brain inflammation, which might be partly mediated by the inhibition of 5-LOX expression and enzymatic activation.
确定米诺环素对大鼠缺血性脑损伤的抗炎作用是否通过抑制5-脂氧合酶(5-LOX)的表达和酶活性来介导。
采用大脑中动脉闭塞法诱导局灶性脑缺血30分钟,随后进行再灌注。在再灌注72小时后测定缺血损伤、内源性IgG渗出、中性粒细胞以及巨噬细胞/小胶质细胞的积聚情况,同时检测5-LOX mRNA表达。在再灌注3小时后测定5-LOX代谢产物(白三烯B4和半胱氨酰白三烯)。
米诺环素(22.5和45毫克/千克,腹腔注射,连续3天)减轻了再灌注72小时后的缺血损伤、IgG渗出以及中性粒细胞和巨噬细胞/小胶质细胞的积聚。它还抑制了再灌注72小时后的5-LOX表达以及再灌注3小时后的白三烯生成。
米诺环素抑制缺血后脑炎症,这可能部分是通过抑制5-LOX表达和酶活性来介导的。