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目的:观察加味孔圣枕中丹对慢性脑缺血致血管性痴呆大鼠胼胝体神经细胞凋亡的影响,探讨本方防治血管性痴呆的可能机制。方法:双侧颈总动脉永久结扎(2VO)法建立慢性脑缺血致血管性痴呆大鼠模型。实验动物随机分为假手术组、模型组、加味孔圣枕中丹组和贝伐单抗组,药物干预30 d。ELISA法测定血清凋亡抑制因子Livin及VEGF水平,TUNEL法检测胼胝体神经细胞凋亡,免疫组织化学染色法测定胼胝体Caspase-3表达。结果:与假手术组比较,模型组大鼠血清VEGF水平、胼胝体神经细胞凋亡指数及Caspase-3蛋白表达显著升高,血清Livin水平显著降低(P<0.05);与模型组比较,加味孔圣枕中丹组大鼠血清Livin及VEGF水平显著升高,胼胝体神经细胞凋亡指数及Caspase-3蛋白表达显著降低(P<0.05)。结论:加味孔圣枕中丹通过升高Livin和VEGF水平,下调Caspase-3表达,发挥抗神经细胞凋亡作用,这可能是其防治慢性脑缺血致血管性痴呆的机制之一。
Objective: To observe the effect of Jiaoshuoshen pill on the apoptosis of corpus callosum neurons in rats with vascular dementia induced by chronic cerebral ischemia, and to explore the possible mechanism of this prescription in preventing and treating vascular dementia. Methods: A rat model of vascular dementia induced by chronic cerebral ischemia was established by permanent bilateral common carotid artery ligation (2VO). The experimental animals were randomly divided into sham-operation group, model group, modified Kongshen pill Zhongdan group and bevacizumab group, drug intervention for 30 days. Serum levels of apoptosis inhibitor Livin and VEGF were measured by ELISA. Apoptosis of corpus callosum was detected by TUNEL method. Caspase-3 expression was detected by immunohistochemical staining. Results: Compared with the sham-operation group, the levels of VEGF, the apoptotic index of the corpus callosum and the expression of Caspase-3 in the model group were significantly increased (P <0.05). Compared with the model group, Serum Livin and VEGF levels were significantly increased in the Sertraline Zhongdan group rats, and apoptosis index and Caspase-3 protein expression in the corpus callosum were significantly decreased (P <0.05). Conclusion: Modified Kong Shengzhen Zhongdan can inhibit the neuronal apoptosis by increasing the levels of Livin and VEGF and down-regulating the expression of Caspase-3, which may be one of the mechanisms of prevention and treatment of vascular dementia induced by chronic cerebral ischemia.