心脑舒通胶囊对血管性痴呆大鼠的神经保护作用

目的]研究心脑舒通胶囊对血管性痴呆大鼠的神经保护作用及部分机制。方法]实验采用成年雄性Wistar大鼠体质量(300±20)g,11周龄,随机分为对照组、模型组和心脑舒通低、高剂量组(14、56 mg/kg)。采用永久性结扎大鼠双侧颈总动脉建立血管性痴呆模型,通过Morris水迷宫检测大鼠的学习和记忆能力,尼氏染色观察神经元的细胞形态变化,免疫组化染色观察海马区小胶质细胞(IBA-1)和星形胶质细胞(GFAP)的表达。结果]心脑舒通各治疗组逃避潜伏期较模型组明显缩短(P0.01),且呈剂量依赖性;心脑舒通高剂量组(56 mg/kg)能明显抑制海马CA1区锥体细胞死亡,及小胶质细胞IBA-1和星形胶质细胞GFAP的表达。结论]心脑舒通胶囊可以改善血管性痴呆大鼠的学习和记忆能力,其机制可能是通过保护海马神经元免受缺血性损伤,同时抑制星型胶质细胞和小胶质细胞活化有关。

Neuroprotective effects of Xinnao Shutong capsule on vascular dementia in rats

Objective] To investigate the neuroprotective effect of Xinnao Shutong capsules (XNST) on vascular dementia in rats.Methods] Adult male Wistar ratsweight (300±20) g, eleven weeks old] were used in this experiment. The rats were randomly divided into control group, model, and two treatment (14, 56 mg/kg XNST) groups. The model of vascular dementia in rats was induced by bilateral common carotid artery ligation (BCCAL). Then throughout a period of two months. XNST was given intragastrically to rats. This was followed by rats'' behaviors evaluation by Morris water maze method to obtain records of their performance regarding learning and memory. The changes of brain cell morphology were observed by Nissl stain. The expression IBA-1and GFAP of the hippocampus were measured with immunohistochemistry staining.Results] XNST improved the ability of learning and memory in vascular dementia rats and prevented the loss of pyramidal cells on CA1 zone in the hippocampus. Moreover, the neuronal cell number was increased dramatically after XNST treatment in dose dependent manner. The number of pyramidal cells in XNST increased significantly than that in model group (P<0.01). XNST (56 mg/kg) can the activation of microglia(IBA-1)expression (P<0.01). XNST (56 mg/kg) could obviously inhibit the activation of astrocytes(GFAP)expression (P<0.01).Conclusion] XNST can improve the learning and memory ability of vascular dementia rats, the underlying mechanism of the effects may be related to its action of preventing neuronal cell of hippocampus against ischemic injury inhibiting the astrocytes and microglia activation.