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目的:观察预应用雷公藤多甙对大鼠局灶性脑缺血再灌注后脑能量代谢和神经运动功能障碍的影响。方法:实验于2001-04/12在郑州大学基础医学院药理学教研室、郑州大学第二附属医院神经内科,郑州市疾病预防控制中心完成。取120只Wistar大鼠随机分为6组:缺血再灌注组,雷公藤多甙45,30,15mg/kg组,尼莫地平组(10mg/kg),假手术组,每组20只。所有动物灌胃给药,1次/d,连灌5d。缺血再灌注组和假手术组灌等体积的生理盐水。末次灌胃后1h,除假手术组不插入尼龙线,其余5组采用线栓法制作大鼠大脑中动脉局灶性缺血再灌注模型,检测各组大鼠脑组织三磷酸腺苷酶活性的变化,并进行神经病学评分(评分越高,功能障碍越重)。结果:120大鼠均进入结果分析。①神经运动功能变化:缺血再灌注组出现明显的神经运动功能障碍,神经病学评分为3.7±0.3;雷公藤多甙15,30,45mg/kg组及尼莫地平组大鼠功能障碍均明显改善,神经病学评分与缺血再灌注组比较差异显著(3.1±0.4,2.7±0.3,2.2±0.2,2.5±0.3,P<0.01)。②三磷酸腺苷酶活性:缺血再灌注组显著低于假手术组(P<0.01),雷公藤多甙各剂量组和尼莫地平组三磷酸腺苷酶活性则高于缺血再灌注组(P<0.05或P<0.01)。结论:在脑缺血再灌注后,脑组织能量代谢障碍,细胞的主动转运功能受损。雷公藤多甙能显著升高三磷酸腺苷酶的活性,改善局灶性脑缺血引起的神经运动功能障碍。
OBJECTIVE: To observe the effects of preconditioning with Tripterygium wilfordii on brain energy metabolism and neuromotor dysfunction after focal cerebral ischemia in rats. METHODS: The experiment was performed at the Department of Pharmacology, Basic Medical College, Zhengzhou University, Department of Neurology, the Second Affiliated Hospital of Zhengzhou University from April to December 2001, and the Center for Disease Control and Prevention of Zhengzhou University. 120 Wistar rats were randomly divided into 6 groups: ischemia-reperfusion group, triptolide 45, 30, 15mg/kg group, nimodipine group (10mg/kg), sham operation group, 20 in each group. All animals were given intragastric administration once a day for 5 days. Ischemia-reperfusion group and sham operation group were given an equal volume of physiological saline. At 1 hour after the last gavage, except for the sham-operated group, the nylon thread was not inserted. The other 5 groups were treated with a thread embolus method to establish a middle cerebral artery ischemic reperfusion model, and the change of ATPase activity in the rat brain was detected. Neurological scores were also performed (the higher the score, the heavier the dysfunction). RESULTS: All 120 rats were involved in the result analysis. 1Changes of neural motor function: Obvious neuromotor dysfunction appeared in ischemic reperfusion group, neurological score was 3.7±0.3; dysfunction in rats of triptolide 15, 30, 45 mg/kg group and nimodipine group was obvious Improvements in neurological scores were significantly different from ischemia-reperfusion group (3.1±0.4, 2.7±0.3, 2.2±0.2, 2.5±0.3, P<0.01). 2 ATPase activity: The ischemia-reperfusion group was significantly lower than the sham-operated group (P<0.01). The adenosine triphosphatase activity of the triptolide and the nimodipine groups was higher than that of the ischemia-reperfusion group (P<0.05 or P<0.01). Conclusion: After cerebral ischemia and reperfusion, the energy metabolism of brain tissue is impaired and the active transport function of cells is impaired. Tripterygium wilfordii can significantly increase the activity of adenosine triphosphatase and improve the neuromotor deficits caused by focal cerebral ischemia.