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背景:银杏叶总黄酮有抗自由基的作用,但其对缺血后脑细胞凋亡的影响尚不十分清楚。目的:研究银杏叶总黄酮对脑缺血诱发的细胞凋亡的抑制作用。设计:以实验动物为观察对象的完全随机设计,对照实验。单位:一所大学的药理学教研室。材料:SD大鼠24只,清洁级,体质量(250±50)g,雌雄各半,实验动物合格证号,皖医实准第01号,随机分为4组,分别为假手术组,模型对照组,银杏叶总黄酮40mg/kg组,银杏叶总黄酮80mg/kg组。方法:实验于2001-10/2002-01在安徽医科大学药理学教研室完成。采用双侧颈总动脉结扎法造成大鼠不完全脑缺血;采用TUNEL法和电镜法观察细胞凋亡;用二苯胺试剂法测定DNA片段含量并测定脑水肿。主要观察指标:银杏叶总黄酮用药后脑缺血致脑皮质细胞凋亡的影响,银杏叶总黄酮用药后脑缺血后DNA片段百分率的影响。结果:结扎双侧颈总动脉可显著诱导脑皮质细胞凋亡,银杏叶总黄酮80mg/kg可显著抑制脑水肿(P<0.05)并减少脑皮质中细胞凋亡数(P<0.01),同时对凋亡细胞超微结构变化有改善作用;银杏叶总黄酮40,80mg/kg可抑制脑缺血诱导的DNA片段的增多(P<0.05,P<0.01)。结论:银杏叶总黄酮对缺血诱导的脑皮质细胞凋亡有抑制作用,并改善凋亡细胞超微结构变化,可减轻缺血组织脑水肿发生并抑制脑缺血诱导的DNA片段的增多?
BACKGROUND: Ginkgo biloba leaf flavonoids have anti-free radical effects, but its effect on brain cell apoptosis after ischemia is not yet clear. Objective: To study the inhibitory effect of Ginkgo biloba leaf flavonoids on apoptosis induced by cerebral ischemia. Design: A completely random design with experimental animals as the subject of observation, controlled experiments. Unit: A university’s Department of Pharmacology. MATERIALS: 24 Sprague-Dawley rats, clean grade, body weight (250 ± 50) g, half male and half male, test animal certificate number, quack doctors actual criteria No. 01, were randomly divided into 4 groups, respectively sham operation group, Model control group, Ginkgo biloba total flavonoids 40mg/kg group, Ginkgo biloba total flavonoids 80mg/kg group. METHODS: The experiment was performed at the Department of Pharmacology, Anhui Medical University from October 2001 to January 2002. Incomplete cerebral ischemia was induced in rats by ligation of bilateral common carotid arteries. Apoptosis was assessed by TUNEL and electron microscopy. DNA fragmentation and brain edema were measured by diphenylamine reagent. MAIN OUTCOME MEASURES: The effect of total flavonoids of Gingko biloba leaves on the apoptosis of cerebral cortex cells after cerebral ischemia, and the effect of Ginkgo biloba L. total flavonoids on the percentage of DNA fragments after cerebral ischemia. RESULTS: Ligation of bilateral common carotid arteries significantly induced cerebral cortical apoptosis. Ginkgo biloba total flavonoids 80 mg/kg significantly inhibited cerebral edema (P<0.05) and decreased the number of apoptotic cells in cerebral cortex (P<0.01). The improvement of the ultrastructural changes of apoptotic cells was observed. Ginkgo biloba leaf flavonoids 40 and 80 mg/kg inhibited the increase of DNA fragments induced by cerebral ischemia (P<0.05, P<0.01). CONCLUSION: Ginkgo biloba leaf flavonoids can inhibit the apoptosis of cerebral cortex cells induced by ischemia, and improve the ultrastructural changes of apoptotic cells. It can reduce the occurrence of cerebral edema in ischemic tissue and inhibit the increase of DNA fragment induced by cerebral ischemia.