种兆忠, 冯亦璞. 丁基苯酞对大脑中动脉阻断后皮层组织中花生四烯酸释放及磷脂酶A2基因表达的影响J. 药学学报, 2000, 35(8): 561-565.
引用本文: 种兆忠, 冯亦璞. 丁基苯酞对大脑中动脉阻断后皮层组织中花生四烯酸释放及磷脂酶A2基因表达的影响J. 药学学报, 2000, 35(8): 561-565.
CHONG Zhao-zhong, FENG Yi-pu. EFFECTS OF DL-3-n-BUTYLPHTHALIDE ON ARACHIDONIC ACID RELEASE AND PHOSPHOLIPASE A2 mRNA EXPRESSION IN CEREBRAL CORTEX AFTER MIDDLE CEREBRAL ARTERY OCCLUSION IN RATSJ. Acta Pharmaceutica Sinica, 2000, 35(8): 561-565.
Citation: CHONG Zhao-zhong, FENG Yi-pu. EFFECTS OF DL-3-n-BUTYLPHTHALIDE ON ARACHIDONIC ACID RELEASE AND PHOSPHOLIPASE A2 mRNA EXPRESSION IN CEREBRAL CORTEX AFTER MIDDLE CEREBRAL ARTERY OCCLUSION IN RATSJ. Acta Pharmaceutica Sinica, 2000, 35(8): 561-565.

丁基苯酞对大脑中动脉阻断后皮层组织中花生四烯酸释放及磷脂酶A2基因表达的影响

EFFECTS OF DL-3-n-BUTYLPHTHALIDE ON ARACHIDONIC ACID RELEASE AND PHOSPHOLIPASE A2 mRNA EXPRESSION IN CEREBRAL CORTEX AFTER MIDDLE CEREBRAL ARTERY OCCLUSION IN RATS

  • 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) 6 h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。Northern blot检测皮层中PLA2基因表达。结果 MCAO后6 h,皮层中AA释放明显增加。于脑缺血后5 min 和120 min,给dl-NBP(10或20 mg.kg-1) 和尼莫地平(0.5 mg.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6 h,皮层中PLA2的基因表达增强。 dl-NBP和d-NBP(10, 20 mg.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。

     

    Abstract: AIM To study the effect of dl-3-n-butylphthalide (dl-NBP) on arachidonic acid(AA) release and phospholipase A2 (PLA2) 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 PLA2 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 mgkg-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 PLA2 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 PLA2 mRNA expression in the ischemic brain tissue in vivo.

     

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