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作 者:唐放鸣[1] 丁允闽[1] 陈幽婷[2] 孙亚锋[2] 王然[2] 张光毅[2] 金国章
机构地区:[1]中国科学院上海药物研究所,上海200031 [2]徐州医学院生物化学与分子生物学研究中心,徐州中国221002
出 处:《中国药理学报》1999年第12期1073-1078,共6页Acta Pharmacologica Sinica
基 金:National Natural Science Foundation of China, № 39870898;Provincial Natural Science Foundation of Jiangsu, № BK97153;Natural Science Foudation of Education Committee of Jiangsu Province, № 98KJB310005
摘 要:目的:研究左旋千金藤立定(SPD)对大鼠纹状体缺血性损伤的拮抗作用。方法:用四动脉结扎形成大鼠前脑缺血模型,焦油紫染色从组织形态观察纹状体中神经元的变化;以纹状体脑片孵育的缺糖缺氧为离体缺血模型,用同位素^(32)P掺入法和比色法测定CCDPK和LDH活性的变化及SPD对它们的影响。结果:缺血30min复灌6h和12h,对照组大鼠纹状体大部分神经元丧失,细胞形态异常;而SPD给药组大鼠纹状体神经元未见明显减少,形态基本正常。SPD减轻缺血时纹状体脑片CCDPK活性的降低及LDH的漏出。缺血30min复灌6h和12h,对照组大鼠纹状体大部分神经元丧失,细胞形态异常;而SPD给药组大鼠纹状体神经元未见明显减少,形态基本正常。SPD减轻缺血时纹状体脑片CCDPK活性的降低及LDH的漏出。结论:SPD对纹状体神经元缺血性损伤有拮抗作用,并可拮抗缺血对纹状体神经元CCDPK活性的抑制及LDH的漏出。AIM: To elucidate the protection of l-stepholidine (SPD) on neuronal morphology and function against the striatal ischemic injury in rat. METHODS: The forebrain ishemia to Sprague Dawley rats was induced with four-vessel occlusion. Histological examination was performed on the dorsolateral striatum with cresyl-violet stain. In striatal slices of rat as an in vitro ischemic model, the activity of calcium/calmodulin-dependent protein kinase Ⅱ (CCDPK) and lactate dehydrogenase (LDH) was examined by the method of 32P-incorporation and colorimetry, respectively. RESULTS: In the SPD-treated groups, most of the neurons in the striatum kept the normal morphological appearance after 30-min ischemia followed by 6-h or 12-h reperfusion. The number of neurons was much more in SPD groups than that in vehicle group. The sparse and abnormal neurons were observed in the vehicle group. SPD attenuated the ischemic effect on the CCDPK activity in striatal slices. In addition, SPD inhibited the leakage of LDH from neurons induced by ischemia in incubated striatal slices. CONCLUSION: SPD protected striatal neurons against ischemic injury and antagonized the inhibitory action onCCDPK activity induced by ischemia. SPD reduced the leakage of LDH from striatal neurons induced by ischemia.
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