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[dl-3-正丁基苯酞对大鼠局灶性脑缺血后迟发性神经元损伤及突触小体内钙的影响]

[Effect of dl-3-n-butylphthalide on delayed neuronal damage after focal cerebral ischemia and intrasynaptosomes calcium in rats].

作者信息

Lin J F, Feng Y P

机构信息

Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing.

出版信息

Yao Xue Xue Bao. 1996;31(3):166-70.

PMID:9206264
Abstract

Effect of dl-3-n-butylphthalide on the size of infarction and behavior changes were investigated after delayed neuronal damage in rats subjected to permanent middle cerebral artery occlusion (MCAO) by the method of Tamura et al, and the scores of behavior were evaluated by the method of Bederson et al. The results show that the size of infarct area was significantly reduced 2 h after MCAO following administration of NBP at the dose of 80, 160 and 240 mg.kg-1, the percentage of reduction of infarct area was 49.0%, 69.5% and 85.1% respectively. Neurological deficit was also improved. The size of infarction and the score of neurological deficit were also reduced significantly following pretreatment with NBP at the dose of 80 mg.kg-1 per day for 7 days by the end of the final dosage 24 h before MCAO or at the single dose of 160 mg.kg-1 1 h before MCAO. The results suggest that NBP has therapeutic and preventive effect on stroke and imply that NBP has the action of attenuating neuronal damage after delayed cerebral injury. In addition, the level of calcium ([Ca2+]i) in rat intrasynaptosomes was determined using fura-2 (a fluorescence indicator) technique. It was found that NBP can not lower the rise of [Ca2+]i induced by 30 mmol.L-1 KCl. However, the effect of NBP on [Ca2+]i overload induced by excitatory amino acid remains to be studied.

摘要

采用Tamura等人的方法,对永久性大脑中动脉闭塞(MCAO)大鼠延迟性神经元损伤后,研究了dl-3-正丁基苯酞对梗死面积大小和行为变化的影响,并采用Bederson等人的方法评估行为评分。结果显示,在MCAO后2小时,给予80、160和240mg·kg-1剂量的NBP后,梗死面积大小显著减小,梗死面积减小百分比分别为49.0%、69.5%和85.1%。神经功能缺损也得到改善。在MCAO前24小时末次给药结束时,以80mg·kg-1的剂量连续7天预处理NBP,或在MCAO前1小时单次给予160mg·kg-1剂量的NBP后,梗死面积大小和神经功能缺损评分也显著降低。结果表明,NBP对中风具有治疗和预防作用,提示NBP具有减轻迟发性脑损伤后神经元损伤的作用。此外,采用fura-2(一种荧光指示剂)技术测定大鼠突触体内的钙([Ca2+]i)水平。发现NBP不能降低由30mmol·L-1 KCl诱导的[Ca2+]i升高。然而,NBP对兴奋性氨基酸诱导的[Ca2+]i超载的影响仍有待研究。

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