三七三醇皂苷对MCAO大鼠BDNF和TrkB表达的影响

Influence of PTS on expressions of BDNF and TrkB in MCAO rats

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 influence of panaxtriol saponins （PTS） on the expressions of brain-derived neurotrophic factor （BDNF） and tyrosine kinase receptor （TrkB） in rat model of cerebral isehemia, and to explore the mechanism of remodeling injured neurons by PTS during cerebral isehemia. Methods An improved EZ Longa method was used to establish the model of middle cerebral artery occlusion （MCAO） in adult male SD rats. Then the rats were randomly divided into the model group （treated with normal saline solution）, the PTS group （treated with Sanqishutong Capsules） and the positive control group （treated with nimodipine） according to EZ Longa values after rat consciousness. The expressions of BDNF and TrkB were observed by immunohistochemical method respectively 3,7 and 28 days after the administration of above medicines in random 6 rats. The rat nerve functions were observed too after the cerebral ischemia. Results Comparing with the normal rats the expresssions of BDNF and TrKB in the rats with MCAO were increased at different time points, and then gradually descended with the time went on. Comparing with the model group the neurological dysfunction induced by cerebral isehemia were relieved obviously and the expressions of BDNF and TrKB were up-regulated in the PTS group. Conclusion PTS can up-regulate the expressions of BDNF and TrkB, through which to prevent the neurons from lesion induced by cerebral ischemia, promote the remodling of neurons and play a role in the treatment of cerebral ischemia.