Open AccessMinocycline inhibits 5‐lipoxygenase activation and brain inflammation after focal cerebral ischemia in rats 1
Author(s) -
CHU Lisheng,
FANG Sanhua,
ZHOU Yu,
YU Guoliang,
WANG Mengling,
ZHANG Weiping,
WEI Erqing
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00578.x
Subject(s) - minocycline , microglia , leukotriene b4 , inflammation , ischemia , arachidonate 5 lipoxygenase , leukotriene , pharmacology , medicine , reperfusion injury , lipoxygenase , endogeny , immunology , anesthesia , chemistry , enzyme , endocrinology , biochemistry , arachidonic acid , asthma , antibiotics
Abstract 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.