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在未预防缺血诱导发热的情况下,银杏叶提取物EGb 761未能在短暂大脑中动脉闭塞后的大鼠中减小脑梗死体积。

The Ginkgo biloba extract, EGb 761, fails to reduce brain infarct size in rats after transient, middle cerebral artery occlusion in conditions of unprevented, ischemia-induced fever.

作者信息

de Lima Keli Carina Miltus, Schilichting Carmen Lúcia Ruiz, Junior Lourival Augusto Cestari, da Silva Flávia Munhoz, Benetoli Arcélio, Milani Humberto

机构信息

Department of Pharmacy and Pharmacology, Health Science Center, Pharmaceutical Sciences Post-Graduation Program, State University of Maringá, Av. Colombo, 5790, CEP 87020-900 Maringá, Paraná, Brazil.

出版信息

Phytother Res. 2006 Jun;20(6):438-43. doi: 10.1002/ptr.1872.

DOI:10.1002/ptr.1872
PMID:16619358
Abstract

There is much biochemical evidence, but very few studies in animal models of stroke in vivo, to suggest that Ginkgo biloba (EGb 761) may offer neuroprotection against regional, ischemic brain damage; additional investigations are needed to ensure future clinical trials. This study reports the effects of EGb 761 given acutely or chronically before ischemia. Rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h and the brain infarct size was assessed 24 h later. Dipyrone (100 mg/kg, i.p.) was injected 30 min before ischemia, and 2.5 and 5.5 h after ischemia, to reduce ischemia-induced fever. EGb 761 (Tebonin) was given acutely (200 mg/kg, p.o., 60 min before ischemia) or chronically (100 mg/kg, p.o., once daily, for 14 days before ischemia). Acute or chronic treatment with EGb 761, either alone or in combination with dipyrone, did not reduce the infarct size compared with saline alone (p > 0.05). Dipyrone failed to prevent ischemia-induced fever during the intra-ischemic period (p > 0.05 vs saline; p < 0.001 vs sham). In the reperfusion phase, dipyrone reduced fever to normothermic levels in the group treated acutely with EGb 761 (p < 0.01 vs saline, p > 0.05 vs sham) but not after chronic EGb 761 (p < 0.01 vs sham), indicating possible pharmacokinetic interaction. In conclusion, within the context of unprevented, ischemia-induced fever, the present results demonstrate that EGb 761 has no significant effect on brain infarct size.

摘要

有许多生化证据表明银杏叶提取物(EGb 761)可能对局部缺血性脑损伤提供神经保护作用,但在体内中风动物模型中的研究却很少;需要进一步研究以确保未来的临床试验。本研究报告了在缺血前急性或慢性给予EGb 761的效果。将大鼠大脑中动脉闭塞(MCAO)2小时,并在24小时后评估脑梗死体积。在缺血前30分钟以及缺血后2.5小时和5.5小时注射安乃近(100mg/kg,腹腔注射)以减轻缺血诱导的发热。EGb 761(金纳多)急性给药(200mg/kg,口服,缺血前60分钟)或慢性给药(100mg/kg,口服,每日一次,缺血前14天)。与单独使用生理盐水相比,EGb 761单独或与安乃近联合进行急性或慢性治疗均未减小梗死体积(p>0.05)。安乃近未能在缺血期预防缺血诱导的发热(与生理盐水相比,p>0.05;与假手术组相比,p<0.001)。在再灌注期,安乃近在急性给予EGb 761治疗的组中将发热降至正常体温水平(与生理盐水相比,p<0.01;与假手术组相比,p>0.05),但在慢性给予EGb 761后则没有(与假手术组相比,p<0.01),这表明可能存在药代动力学相互作用。总之,在未预防的缺血诱导发热的情况下,目前的结果表明EGb 761对脑梗死体积没有显著影响。

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