Minocycline inhibits 5-lipoxygenase activation and brain inflammation after focal cerebral ischemia in rats  

作　　者：Li-sheng CHU San-hua FANG Yu ZHOU Guo-liang YU Meng-ling WANG Wei-ping ZHANG Er-qing WEI 

机构地区：[1]Department of Pharmacology, School of Medicine, Zhejiang University, Hangzhou 310058, China [2]Department of Physiology, Zhejiang Chinese Medical University, Hangzhou 310053, China

出　　处：《Acta Pharmacologica Sinica》2007年第6期763-772,共10页中国药理学报（英文版）

基　　金：the National Natural Science Foundation of China(№ 30371637);the Scientific Foundation of the Education Ministry of China(№ 20050335105)

摘　　要：Aim： To determine whether the anti-inflammatory effect of minocycline on postischemic brain injury is mediated by the inhibition of 5-1ipoxygenase （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 B4 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.Aim： To determine whether the anti-inflammatory effect of minocycline on postischemic brain injury is mediated by the inhibition of 5-1ipoxygenase （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 B4 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.

关 键 词：MINOCYCLINE 5-1ipoxygenase LEUKOTRIENE focal cerebral ischemia INFLAMMATION 

分 类 号：R97[医药卫生—药品]