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目的:探讨丹参酮II A对局灶性脑缺血大鼠的神经保护作用及其机制。方法:大鼠局灶性脑缺血模型采用持续性大脑中动脉线栓法制作而成。丹参酮II A剂量2mg/kg.d,4mg/kg.d ip。持续栓塞3 h后进行神经行为学评分,6 h后断头取脑,分离皮层和化海马组织,分光光度法测定丙二醛(malondialdehyde,MDA)含量和超氧化物歧化酶(superoxide dismutase,SOD)以及谷胱甘肽过氧物酶(GPX)活性的变化;运用高效液相色谱法测定不同组大鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量。结果:①缺血组动物均有不同程度的神经功能缺损,评分均在3分以上,而丹参酮IIA治疗组动物检测提尾时不能伸展对侧前肢,评分均为为2分以下,与缺血组动物比较有显著差异;②丹参酮II A可减少MDA的生成,增加SOD、GPX活性;③持续栓塞6h后,大鼠皮层和海马组织谷氨酸和γ-氨基丁酸的含量增加,丹参酮II A可减少局灶性脑缺血大鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量。结论:丹参酮II A在局灶性脑缺血大鼠可发挥神经保护作用,其可能的作用机制包括抗氧化作用以及对兴奋性氨基酸和抑制性氨基酸的调节作用。
Objective: To explore the neuroprotective effect of tanshinone II A on focal cerebral ischemia in rats and its mechanism. Methods: The model of focal cerebral ischemia in rats was made by the method of continuous middle cerebral artery occlusion. Tanshinone II A dose of 2mg / kg.d, 4mg / kg.d ip. The neurobehavioral score was maintained for 3 h after embolization. After 6 h, the brain was decapitated and the cortex and hippocampus were separated. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by spectrophotometry ) And glutathione peroxidase (GPX). The content of glutamate and γ-aminobutyric acid in different groups of cortex and hippocampus were determined by high performance liquid chromatography. Results: ① The animals in the ischemic group all had different degrees of neurological deficits, with the scores above 3, while the animals in the tanshinone IIA group could not extend the contralateral forelimbs at the end of the test. All the scores were below 2, (2) Tanshinone IIA can reduce the formation of MDA and increase the activities of SOD and GPX; (3) The levels of glutamate and γ-aminobutyric acid in the cortex and hippocampus of rats increased continuously after 6h of embolization, A can reduce the levels of glutamate and gamma-aminobutyric acid in the cortex and hippocampus of focal cerebral ischemia rats. CONCLUSION: Tanshinone II A can play a neuroprotective role in focal cerebral ischemia in rats, and its possible mechanism of action includes anti-oxidative effects and its regulation on excitatory amino acids and inhibitory amino acids.