Cerebral protective reaction of ginkgo biloba extract in normothermia cerebral ischemic rat
- VernacularTitle:银杏叶制剂对正常脑温脑缺血大鼠的脑保护作用
- Author:
Xiaoying QIU
;
He WANG
;
Lisha YANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(13):243-245
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: In the researches of Ginkgo Biloba Extract(GBE) in the treatment of cerebra ischemia, because of the application of generally anaesthesia medication that may induce the alteration of cerebral temperature, the accuracy of the results may be affected.OBJECTIVE: To investigate the impact of domestic GBE on antioxidase and lipid peroxide of cerebral ischemic reperfusion tissue as well as the water content of ischemic brain tissue under normothermia.DESIGN: A randomised controlled trial.SETTING and MATERIALS: Study was conducted in the Tongji Medical University of Huazhong Science and Technology University. A total of 24 Wistar rats with a mass from 250 g to 300 g were randomly allocated into sham-operation group ( n = 8 ), cerebral ischemia control group ( n = 8) and cerebral ischemia GBE treatment group( n = 8) . The animal model of normothermia rat with left middle cerebral artery ischemia for 2 hours and reperfusion for 2 hours was prepared with the reference of Nagasawa method in the animals of control group and treatment group for contrast study.INTERVENTIONS: The cerebral temperature of the rats was reflected by the temperature of the temporal muscle. The temperature-measuring probe was embedded into the deep part of the left temporal muscle closed to osseous ectoblast. The temperature was continuously monitored by semiconductor oxide temperature sensor. The temperature of the head was heated with 60 W filament lamp and adjusted by automatic double-controlling craniocerebral cooling instrument to maintain the cerebral temperature at normothermia level of 36.5 ℃ - 37 ℃. The normothermia cerebral ischemic reperfusion injury rat model was established according to the design. GBE injection was injected respectively into abdominal cavity in the rats of cerebral ischemia GBE treatment group at the following time point: 12 hours, 8 hours and 4 hours before operation, immediately after cerebral ischemia and immediately after reperfusion, with 3 mL each time and 5 times in total. Same times and dose of normal saline was injected into the abdominal cavity in the rats of both control group and sham-operation groups.MAIN OUTCOME MEASURES: Superoxide dismutase (SOD), glutathione peroxidase(GSH-Px), reduced glutathione(GSH), malondialdehyde(MDA)and water contents in the cerebral ischemic tissue.RESULTS: The levels of SOD, GSH-Px and GSH in cerebral ischemia control group were(73.35 ± 12. 86) NU/mg, (167.37 ±54.34) μkat/g and (196. 84 ± 22.75) μg/g respectively, which significantly lower than that (96. 02± 16. 83) NU/mg, (338.57±84.02) μkat/g and(337.51± 34. 89) μg/g of sham-operation group( P ＜ 0. 01 or P ＜ 0.05) . The SOD, GSH-Px and GSH levels of cerebral isehemia GBE treatment group were (87.24± 15.03) NU/mg, (316. 56 ±93.52) μkat/g and(263.16±28.54) μg/g, which significantly higher than that of cerebral ischemia control group(P ＜ 0.01 or P ＜ 0.05) .The MDA level of cerebra ischemia control group was (308.34 ± 26.81 ) nmol/g, which significantly higher than that(101.46 ± 10.97) nmol/g of sham-operation group( P ＜ 0.01 ) .The MDA level of cerebral ischemia GBE treatment group was(125.86± 13.90) nmol/g, which was significantly lower than that of sham-operation group ( P ＜ 0.01 ) . The water content of cerebral ischemia control group was(80. 45 ± 0.44)%, which was significantly higher than that (78.20 ± 0. 25 ) % of sham-operation group ( P ＜ 0.01 ) . The water content of cerebral ischemia GBE treatment group was(79.63 ± 0.46) %, which was significantly lower than that of cerebral ischemia control group( P ＜ 0.05).CONCLUSION: Domestic GBE can inhibit the excessive production of free radicals and the lipid peroxidation during cerebral ischemia and reduce cerebral oedema and the destruction of blood-brain barrier to protect cerebral ischemic tissues under cerebral normothermia.
