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作 者:陈当 周梅[2] 孙铁[2] 冯秀玲[2] 郭莲军[2]
机构地区:[1]湖北省英山县人民医院神经科,湖北英山438700 [2]华中科技大学同济医学院药理学系,湖北武汉430030
出 处:《中国医院药学杂志》2014年第8期616-620,共5页Chinese Journal of Hospital Pharmacy
基 金:国家重大创新平台重点资助新药研发项目(基金号:2009ZX09301-014);中央高校基本科研业务费专项资金资助项目(编号:2011TS073)
摘 要:目的:探讨蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注损伤皮层和海马钙蛋白酶活性的影响。方法:采用大鼠大脑中动脉栓塞2 h后,再灌注24 h,即局灶性脑缺血-再灌注损伤模型,用吸光光度法观察缺血侧和非缺血侧皮层与海马钙蛋白酶活性的变化,并探讨蝙蝠葛酚性碱对其活性的影响。结果:大鼠局灶性脑缺血-再灌注后,缺血侧皮层和海马钙蛋白酶活性均显著升高,蝙蝠葛酚性碱(10,20 mg·kg-1)能依剂量降低缺血侧皮层和海马的钙蛋白酶活性。结论:蝙蝠葛酚性碱能降低缺血-再灌注损伤大鼠缺血侧皮层和海马钙蛋白酶的活性,可能是其减轻脑缺血损伤所致神经细胞凋亡或死亡的机制之一。OBJECTIVE To investigate the effect of PAMd on Calpain activities in local cerebral ischemia (2h) reperfusion (24h) model of rats. METHODS The animal model was induced by transient occlusion of the middle cerebral artery, PAMd was given immediately after reperfusion, then it was given in 22 h after reperfusion again. The dose of PAMd was 5, 10, 20 mg·kg^-1 , respectively. The activities of Calpain in hippocampus and cortex were determined by spectrophotography. RE- SULTS The Calpain activities of ischemic cortex increased significantly to (2. 81 ±0. 38)△A·mg^-1(protein), and the Calpain activity of normal cortex was (1.68 ± 0. 21) △A·mg^-1 (protein). Given PAMd (10, 20 mg·kg^-1) after I-R, the Calpain activ- ities of ischemic cortex decreased to (2. 06± 0. 47) and (1.98 ± 0. 34) △A·mg^-1 (protein) respectively. The Calpain activities of ischemic hippocampus increased significantly to (2.96 ±0. 41) △A·mg^-1(protein). Given PAMd (10, 20 mg·kg^-1 ) after I- R, the Calpain activities of isehemic hippoeampus decreased to (2. 28 ± 0. 29)and (2. 08 ±0. 34)△A·mg^-1 (protein) respectively. CONCLUSION The results showed above proved that PAMd could decrease the Calpain activities of ischemic cortex and hippocampus in I-R rats, then reduce the apoptosis or death of neurons after brain ischemia.
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