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目的:研究参银复智制剂对拟血管性痴呆(vascular dementia,VD)大鼠海马CA1区的改善作用及相关机制。方法:通过反复夹闭再通大鼠双侧颈总动脉制作拟血管性痴呆大鼠模型,按照1ml/100g体重灌胃给药,每天1次,连续30天,假手术组和模型组灌胃生理盐水,高、中、低剂量组分别灌胃2.32g,1.16g,0.58g生药/ml的参银复智混悬液1ml/100g,阳性药物组灌胃0.024mg成药/ml喜得镇混悬液1ml/100g。通过苏木素-伊红和刚果红染色比较使用大、中、小剂量参银复智制剂治疗后的海马CA1区细胞形态学改变和细胞数目及淀粉样蛋白沉淀情况,Western blot检测相关蛋白的表达。结果:模型组海马CA1区锥体细胞数明显减少,其顶树突缩短甚至消失,淀粉样蛋白沉积明显,应用参银复智制剂能减轻海马CA1区的损伤。参银复智制剂大、中剂量组的细胞数量和淀粉样蛋白沉淀与小剂量组相比有明显改善。Western blot检测发现,参银复智大、中剂量组可明显降低血管痴呆模型大鼠海马β-淀粉样蛋白(β-amyloid,Aβ)、β-淀粉样前体蛋白裂解酶1(β-site amyloid precursor protein cleaving enzyme 1,BACE1)、淀粉样前体蛋白(amyloid protein precursor,APP),但对早老素1(presenilin 1,PS1)表达没有明显影响;可明显提高模型大鼠海马神经内肽酶(neprilysin,NEP)和胰岛素降解酶(insulin-degrading enzyme,IDE)的表达。结论:参银复智制剂能发挥血管痴呆型大鼠的海马CA1区的保护作用,降低海马Aβ的沉积,这可能是其改善VD大鼠学习记忆障碍的重要机制。
Objective: To study the effect of Shenyinbulai on improving hippocampal CA1 region of vascular dementia (VD) rats and its related mechanism. Methods: The rat model of vascular dementia was established by repeated clipping of bilateral common carotid arteries in rats. The rats were administered intragastrically with 1ml / 100g body weight once daily for 30 days. The rats in sham operation group and model group Saline, high, medium and low dose groups were gavage 2.32g, 1.16g, 0.58g crude drug / ml of Shenyinfukosin suspension 1ml / 100g, positive drug group gavage 0.024mg drug / ml happy town mixed Suspension 1ml / 100g. The morphological changes of hippocampal CA1 region, the number of cells and the deposition of amyloid protein were observed by hematoxylin-eosin and Congo red staining, and the expression of related protein was detected by Western blot. Results: The number of pyramidal cells in hippocampal CA1 region of model group decreased significantly, the apical dendrites shortened or even disappeared, and the amyloid protein deposition was obvious. The application of Shenyinbaizhi can relieve the damage of hippocampal CA1 region. Shenyinbulai preparations large and medium dose group of cells and amyloid deposition in the number of cells compared with the small dose group has significantly improved. The result of Western blot showed that Shenyinbubai large and medium dose groups could significantly decrease the levels of β-amyloid (Aβ), β-site amyloid precursor protein cleaving enzyme 1, BACE1 and amyloid protein precursor (APP), but had no obvious effect on the expression of presenilin 1 (PS1) (neprilysin, NEP) and insulin-degrading enzyme (IDE). Conclusion: Shenyinfumingzhi can exert the protective effects of hippocampus CA1 in vascular dementia rats and decrease the deposition of Aβ in hippocampus, which may be an important mechanism of improving learning and memory impairment in VD rats.