摘要
BACKGROUND： Some researches suggest that induced cyclooxygenase-2 （COX-2） can cause brain injury through a series of ways at the phase of cerebral ischemia/hypoxia. Plasminogen activator inhibitor type-1 （PAl-1） is a kind of inhibitor of serine stretch protein enzyme and is able to protect cell surface and microvascular basement membrane from degradation of protease and also protect contact surface among cells so as to maintain intecjrality of tissue structure. However, correlation of protective effect of flunar z ne on bran w th COX-2 and PAl-1 should be studied further. OBJECTTVE ： To observe the effect of flunarizine on expressions of COX-2 and PAl-1 protein in forebrain and degree of brain injury among gerbils after cerebral ischemia. DESIGN ： A randomized controlled animal study SETTING： Department of Neurology, the Second Xiangya Hospital of Central South University; Department of Neurology, Mawangdui Hospital of Hunan Province. MATERIALS： A total of 40 healthy gerbils, of both genders, aged 9 months, weighing （90±10） g, were selected in this study. Anti-COX-2 multi-antibody, anti-PAl-1 multi-antibody, SABC immunohistochemical kit and DAB kit were provided by Wuhan Boster Biological Engineering Co., Ltd.; and flunarizine capsule was provided by Xi＇an Yangsen Pharmaceutical Company （batch number： 041018726, dosage： 5 mg/pill）. METHODS： The experiment was carded out in Laboratory of Mental Disease, Hunan Provincial Geriatrics Institute affiliated by Hunan Provincial Mawangdui Hospital from January 2004 to March 2005. （1） All gerbils were randomly divided into cerebral ischemia group, flunarizine intervention group, sham operation group and norma control group with 10 in each group. Gerbils in normal control group were only cut off their heads. Gerbils in sham operation group were only dissected their bilateral common carotid arteries and sacrificed 1 day later. Gerbils in cerebral ischemia group and flunarizine intervention group were anesthetized, centrally cut open ski
BACKGROUND： Some researches suggest that induced cyclooxygenase-2 （COX-2） can cause brain injury through a series of ways at the phase of cerebral ischemia/hypoxia. Plasminogen activator inhibitor type-1 （PAl-1） is a kind of inhibitor of serine stretch protein enzyme and is able to protect cell surface and microvascular basement membrane from degradation of protease and also protect contact surface among cells so as to maintain intecjrality of tissue structure. However, correlation of protective effect of flunar z ne on bran w th COX-2 and PAl-1 should be studied further. OBJECTTVE ： To observe the effect of flunarizine on expressions of COX-2 and PAl-1 protein in forebrain and degree of brain injury among gerbils after cerebral ischemia. DESIGN ： A randomized controlled animal study SETTING： Department of Neurology, the Second Xiangya Hospital of Central South University; Department of Neurology, Mawangdui Hospital of Hunan Province. MATERIALS： A total of 40 healthy gerbils, of both genders, aged 9 months, weighing （90±10） g, were selected in this study. Anti-COX-2 multi-antibody, anti-PAl-1 multi-antibody, SABC immunohistochemical kit and DAB kit were provided by Wuhan Boster Biological Engineering Co., Ltd.; and flunarizine capsule was provided by Xi＇an Yangsen Pharmaceutical Company （batch number： 041018726, dosage： 5 mg/pill）. METHODS： The experiment was carded out in Laboratory of Mental Disease, Hunan Provincial Geriatrics Institute affiliated by Hunan Provincial Mawangdui Hospital from January 2004 to March 2005. （1） All gerbils were randomly divided into cerebral ischemia group, flunarizine intervention group, sham operation group and norma control group with 10 in each group. Gerbils in normal control group were only cut off their heads. Gerbils in sham operation group were only dissected their bilateral common carotid arteries and sacrificed 1 day later. Gerbils in cerebral ischemia group and flunarizine intervention group were anesthetized, centrally cut open ski
基金
the Scientific and Technological Foundation of Hunan Public Health Bureau,No. B2003-132
