摘要
目的 研究丁基苯酞 (dl NBP) ,d NBP和l NBP对大脑中动脉阻断 (MCAO) 6h后缺血区皮层中花生四烯酸 (AA)释放及磷脂酶A2 (PLA2 )基因表达的影响。方法 阻断大脑中动脉起始部造成局灶性脑缺血模型。HPLC检测AA。Northernblot检测皮层中PLA2 基因表达。结果 MCAO后 6h ,皮层中AA释放明显增加。于脑缺血后 5min和 12 0min ,给dl NBP(10或 2 0mg·kg- 1)和尼莫地平 (0 5mg·kg- 1)可显著抑制AA的释放。d NBP和l NBP作用比较 ,显示d NBP有与dl NBP相似的作用 ,而l NBP则无明显影响。Northern印迹结果表明 ,脑缺血 6h ,皮层中PLA2 的基因表达增强。dl NBP和d NBP(10 ,2 0mg·kg- 1,ip)皆可使表达降低 ,而l NBP对缺血脑组织中PLA2 的基因表达的升高无明显影响。结论 dl NBP和d NBP可抑制MCAO后脑组织中AA释放和PLA2 的基因表达。
AIM To study the effect of dl -3-n-butylphthalide ( dl -NBP) on arachidonic acid(AA) release and phospholipase A_2 (PLA_2) mRNA in cerebral cortex of rats subjected to focal cerebral ischemia. METHODS Focal cerebral ischemia was induced by inserting a monofilament nylon suture into the internal carotid artery and blocking the origin of the middle cerebral artery. AA was determined with high performance liquid chromatography (HPLC). The PLA_2 mRNA expression was evaluated by Northern blot analysis. RESULTS Six hours of cerebral ischemia induced AA release in the ischemic cerebral cortex. dl -NBP (10 or 20 mg·kg -1 ) and nimodipine (0 5 mg·kg -1 ) given intraperitoneally 5 min and 120 min again after the onset of ischemia significantly reduced AA concentration in the cerebral cortex ( P <0 01). d -NBP, but not l -NBP, decreased AA release in the brain after middle cerebral artery occlusion. The expression of PLA_2 mRNA in cerebral cortex induced by cerebral ischemia was also inhibited by dl -NBP and d -NBP (10 or 20 mg·kg -1 , ip). CONCLUSION dl -NBP and d -NBP inhibited AA release and PLA_2 mRNA expression in the ischemic brain tissue in vivo .
出处
《药学学报》
CSCD
北大核心
2000年第8期561-565,共5页
Acta Pharmaceutica Sinica
基金
SupportedbyagrantfromtheStateScienceandTechnologyCommission
No . 94 2D 0 1and partialsupportfromtheNationalScienceFoundati
关键词
丁基苯酞
花生四烯酸
磷脂酶A2
脑缺血
尼莫地平
dl -3-n-butylphthalide
arachidonic acid
phospholipase A_2
cerebral ischemia
nimodipine CLC number:R966
R743.31
Q34413
Document code:A
Article ID:0513-4870(2000)08-0561-05
