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目的探讨川芎嗪预处理对沙鼠前脑缺血再灌注损伤的保护作用及机制。方法雄性沙鼠随机分为对照、脑缺血再灌注、缺血预处理、川芎嗪预处理组,参照Kirino法制备脑缺血再灌注模型,Kitagawa法制备脑缺血预处理模型,HE染色法观察海马区神经细胞形态变化,免疫组织化学法检测神经胶质纤维酸性蛋白(GFAP)表达,原位缺口末端标记法(TUNEL)检测神经细胞凋亡情况,4-pellet taking test(4-PTT)旱路迷宫法测试动物学习记忆功能。结果与脑缺血再灌注组比较,缺血预处理和川芎嗪预处理组中存活神经元密度(12.93±3.17,18.74±4.21)增加;GFAP(8.50±1.25,12.72±1.38)表达增加,凋亡神经细胞数量(16.50±5.25,9.72±3.38)下降;参照记忆指数和工作记忆指数得到改善(P均<0.05)。结论川芎嗪预处理可改善脑缺血再灌注沙鼠的学习记忆功能,其机制与增强星形胶质细胞活性、减少神经细胞凋亡有关。
Objective To investigate the protective effect of ligustrazine on forebrain ischemia-reperfusion injury in gerbils and its mechanism. Methods Male gerbils were randomly divided into control, cerebral ischemia-reperfusion, ischemic preconditioning and ligustrazine preconditioning. Cerebral ischemia / reperfusion model was established by Kirino method. Cerebral ischemic preconditioning model was established by Kitagawa method. HE staining The morphological changes of neurons in the hippocampus were observed. The expression of glial fibrillary acidic protein (GFAP) was detected by immunohistochemistry. The apoptosis of neurons was detected by 4-pellet taking test (TUNEL) Dry road maze test animal learning and memory function. Results Compared with cerebral ischemia-reperfusion group, the survival neuron density (12.93 ± 3.17, 18.74 ± 4.21) increased in ischemic preconditioning and ligustrazine preconditioning groups; the expression of GFAP (8.50 ± 1.25,12.72 ± 1.38) The number of apoptotic nerve cells (16.50 ± 5.25, 9.72 ± 3.38) decreased; the reference memory index and working memory index were improved (all P <0.05). Conclusion Tetramethylpyrazine preconditioning can improve the learning and memory function of gerbils with gerbil ischemia reperfusion. Its mechanism is related to the enhancement of the activity of astrocytes and the reduction of neuronal apoptosis.