Objective To investigate the protective mechanism of Naoluoxintong Prescription, a representative qi-tonifying, blood-activating, and collateral-dredging prescription, in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) with qi deficiency and blood stasis.Methods A total of 72 male Sprague-Dawley rats were divided into normal group, model group, Naoluoxintong group, and Tongxinluo group using a random number table, with 18 rats in each group.Each group was further divided into 1-, 3-, and 7-day groups using a random number table, with 6 rats in each group.Qi-deficiency and blood-stasis syndrome was simulated by starvation, fatigue, hypoxia, and high-fat diet, and with reference to the modified LONGA method, the suture method was used to establish a rat model of MCAO/R.The concentration of Naoluoxintong solution was 0.26 g/mL and that of Tongxinluo solution was 0.02 g/mL.The rats in the Naoluoxintong group and Tongxinluo group were administered Naoluoxintong and Tongxinluo, respectively, by gavage at a dose of 10 mL/kg every day, and those in the normal group and model group were given an equal volume of normal saline by gavage.RT-PCR was used to measure the expression of Wnt3a, Wnt5a, and β-Catenin in the hippocampus and the frontal and parietal cortex.Results Compared with the normal group, the model group had significant increases in the expression of Wnt3a, Wnt5a, and β-Catenin in the hippocampus and the frontal and parietal cortex in the ischemic hemisphere on days 1, 3, and 7 (P<0.05).Compared with the model group, the Tongxinluo group and the Naoluoxintong group had a significant increase in the expression of Wnt3a, Wnt5a, and β-Catenin in the hippocampus and the frontal and parietal cortex in the ischemic hemisphere on days 1, 3, and 7 (P<0.05).Compared with the Tongxinluo group, the Naoluoxintong group had a significant increase in the expression of Wnt3a, Wnt5a, and β-Catenin in the hippocampus and the frontal and parietal cortex in the ischemic hemisphere on days 1, 3, and 7 (P<0.05).Conclusion Naoluoxintong can regulate the proliferation and differentiation of neural stem cells after cerebral ischemia, possibly by upregulating the expression of Wnt3a, Wnt5a, and β-Catenin.%目的 探讨益气活血通络法代表方脑络欣通对气虚血瘀型中脑动脉阻塞再灌注(middle cerebral artery occlusion-reperfusion,MCAO/R)模型大鼠的保护机制.方法 采用随机数字表法将雄性SD大鼠分成正常组、模型组、脑络欣通组和通心络组,每组18只.按随机数字表法将各组再分成1、3、7 d组,每时间节点组6只.气虚血瘀证采用饥饿、疲劳、缺氧及高脂饮食等多因素模拟,线栓法制作MCAO/R模型参照改良后的LONGA法.脑络欣通配制成浓度为0.26 g/mL的溶液,通心络配制成浓度为0.02 g/mL的溶液.按每日10 mL/kg灌胃给药.正常组及模型组按等容量生理盐水灌胃.利用RT-PCR检测各组大鼠海马及额顶叶皮质Wnt3a、Wnt5a和β-Catenin的表达.结果 与正常组比较,模型组大鼠缺血侧海马和额顶叶皮质Wnt3a、Wnt5a、β-Catenin在1、3、7 d表达水平显著上调(P<0.05);与模型组比较,通心络组、脑络欣通组大鼠缺血侧海马和额顶叶皮质Wnt3a、Wnt5a和β-Catenin在1、3、7 d表达水平显著上调(P<0.05);与通心络组比较,脑络欣通组大鼠缺血侧海马和额顶叶皮质Wnt3a、Wnt5a和β-Catenin在1、3、7 d表达水平显著上调(P<0.05).结论 脑络欣通可能通过上调Wnt3a、Wnt5a以及β-Catenin的表达调节脑缺血后神经干细胞的增殖分化.
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