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

• Published in: Phytotherapy research 2006-06, Vol.20 (6), p.438-443
• Main Authors: de Lima, Keli Carina Miltus, Schilichting, Carmen Lúcia Ruiz, Junior, Lourival Augusto Cestari, da Silva, Flávia Munhoz, Benetoli, Arcélio, Milani, Humberto
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; Biological and medical sciences; brain infarct size; Brain Ischemia - complications; Brain Ischemia - drug therapy; dipyrone; Dipyrone - therapeutic use; EGb 761; fever; Fever - drug therapy; Fever - etiology; General pharmacology; Ginkgo biloba; Infarction, Middle Cerebral Artery - prevention & control; Male; Medical sciences; Neuroprotective Agents - therapeutic use; Pharmacognosy. Homeopathy. Health food; Pharmacology. Drug treatments; Phytotherapy; Plant Extracts - therapeutic use; Rats; Rats, Wistar
• ISSN: 0951-418X; 1099-1573
• DOI: 10.1002/ptr.1872

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. Copyright © 2006 John Wiley & Sons, Ltd.