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目的观察三七三醇皂苷(PTS)对脑缺血大鼠模型脑源性神经营养因子(BDNF)及其酪氨酸激酶受体B(TrkB)表达的影响,揭示PTS对脑缺血受损神经元的重塑作用机制。方法选取成年雄性SD大鼠,采用改良的EZ Longa方法建立大脑中动脉缺血(MCAO)大鼠模型,根据清醒后所得Longa评分随机分为模型组(生理盐水)、三七三醇皂苷组(三七舒通胶囊)和阳性对照组(尼莫地平),分别于给药后3、7、28 d随机取大鼠6只,通过免疫组织化学法观察BDNF和TrkB的表达,并观察大鼠脑缺血后的神经功能变化。结果与正常组比较,术后各时间点脑组织BDNF和TrkB表达变化均有增高,并随时间的迁延呈下降的趋势。与模型组比较,三七三醇皂苷组能明显改善脑缺血的神经功能缺失症状,并能上调皮质中BDNF和TrkB蛋白的表达水平。结论三七三醇皂苷能上调脑缺血后BDNF和TrkB蛋白的表达,可能通过上调BDNF和TrkB表达对脑缺血神经元损伤起保护作用,促进神经元的重塑,发挥其对脑缺血的治疗作用。
Objective To observe the effect of PTS on the expression of brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor B (TrkB) in the rat model of cerebral ischemia, and to reveal the impairment of PTS on cerebral ischemia. Neuronal remodeling mechanism. Methods Adult male Sprague-Dawley rats were selected to establish a middle cerebral artery occlusion (MCAO) rat model using the modified EZ Longa method. They were randomly divided into model group (normal saline) and triclosan saponin group according to the Longa score obtained after waking up. (3) Qiqi Shutong capsule) and positive control group (nimodipine). Six rats were randomly selected at 3, 7, and 28 days after administration, and the expression of BDNF and TrkB was observed by immunohistochemistry and the rats were observed. Neurological changes after cerebral ischemia. Results Compared with the normal group, the changes of BDNF and TrkB expression in brain tissue at all time points were increased, and the time delays showed a tendency to decline. Compared with the model group, the PTS group significantly improved neurological deficits in cerebral ischemia and up-regulated the expression of BDNF and TrkB in the cortex. Conclusion PRP can up-regulate the expression of BDNF and TrkB protein after cerebral ischemia, and may up-regulate the expression of BDNF and TrkB, protect neurons from damage of cerebral ischemia, promote the remodeling of neurons, and exert their effects on cerebral ischemia. Therapeutic effect.