夏天无对血管性痴呆模型大鼠神经行为学及海马CA1区MVD、VEGF蛋白表达的影响
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摘要
目的:观察夏天无对血管性痴呆模型大鼠学习记忆及海马CA1区MVD、VEGF蛋白表达的影响。方法:大鼠随机分为假手术组、模型组及夏天无组。血管性痴呆模型建立后连续给药30d。免疫组织化学法检测微血管密度及VEGF蛋白表达的变化。结果:夏天无组较模型组自第3天起平均逃避潜伏期缩短(P <0.05),后2天其平均逃避潜伏期明显缩短,穿越平台次数明显增加(P <0.01);夏天无组海马CA1区血管数量有所增加,VEGF阳性细胞数量有所增加(P <0.05)。结论:夏天无对血管性痴呆学习记忆障碍有一定改善作用,其机制可能是通过增强VEGF表达,一方面对海马CA1区神经元直接起保护作用,另一方面诱导缺血区侧枝新血管形成,改善血液循环,对神经元起间接保护作用。
Objective: To observe efficacy of Xiatianwu( 夏天无) on neurobehavioral and expression of MVD and VEGF protein in hippocampal CA1 region in vascular dementia model rats. Methods: All rats were randomly divided into 3 groups: the sham operation group, the model group and the Xiatianwu group. The vascular dementia model was intervened with continuous administration for 30 days. Microvessel density and the expression of VEGF protein were detected by immunohistochemistry. Results: Compared with the model group, the average escape avoidance period of the Xiatianwu group was shortened from the third day(P<0.05). It was significantly shortened after 2 days(P<0.01), and the number of platforms was increased significantly(P<0.01). The number of blood vessels and VEGF-positive cells were increased in the hippocampal CA1(P<0.05). Conclusion: Xiatianwu can inprove the learning and memory impairment of vascular dementia. The mechanism may be to directly protect neurons in hippocampal CA1 region by enhancing VEGF expression, and improve blood circulation by inducing collateral neovascularization in ischemic region for indirect protection of neurons.
Objective: To observe efficacy of Xiatianwu( 夏天无) on neurobehavioral and expression of MVD and VEGF protein in hippocampal CA1 region in vascular dementia model rats. Methods: All rats were randomly divided into 3 groups: the sham operation group, the model group and the Xiatianwu group. The vascular dementia model was intervened with continuous administration for 30 days. Microvessel density and the expression of VEGF protein were detected by immunohistochemistry. Results: Compared with the model group, the average escape avoidance period of the Xiatianwu group was shortened from the third day(P<0.05). It was significantly shortened after 2 days(P<0.01), and the number of platforms was increased significantly(P<0.01). The number of blood vessels and VEGF-positive cells were increased in the hippocampal CA1(P<0.05). Conclusion: Xiatianwu can inprove the learning and memory impairment of vascular dementia. The mechanism may be to directly protect neurons in hippocampal CA1 region by enhancing VEGF expression, and improve blood circulation by inducing collateral neovascularization in ischemic region for indirect protection of neurons.
引文
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