丁苯酞对急性动脉粥样硬化性脑梗死大鼠神经功能的影响

Effect of butylphthalide on neural function in atherosclerotic ACI rats

目的探究丁苯酞对急性动脉粥样硬化性脑梗死大鼠神经功能的影响。方法随机选择SPF级SD大鼠42只分为对照组,模型组和丁苯酞组(n=14),对照组使用正常饲料并暴露颈动脉不结扎,模型组和丁苯酞组建立动脉粥样硬化模型和脑梗死模型后给药。采用改良神经功能缺损评分(mNSS)评估神经功能,检测外周血神经元特异性烯醇化酶(NSE)、内皮素1、磷脂酰肌醇3激酶(PI3K)、蛋白激酶B(Akt)、血管内皮生长因子(VEGF)mRNA和蛋白表达。结果模型组mNSS、脑梗死体积、凋亡指数、NSE和内皮素1水平明显高于对照组,血管数量、PI3K、Akt、VEGF mRNA和蛋白明显低于对照组,差异有统计学意义(P<0.05)。丁苯酞组mNSS、脑梗死体积、凋亡指数、NSE和内皮素1水平明显低于模型组[(5.86±1.02)分vs(12.85±2.16)分,(14.38±2.43)%vs(36.45±4.78)%,(20.43±2.56)%vs(46.75±3.72)%,(11.24±1.53)μg/L vs(15.86±2.24)μg/L,(40.35±4.74)μg/L vs(51.17±6.21)μg/L,P<0.05)],血管数量、PI3K、Akt和VEGF mRNA和蛋白明显高于模型组,差异有统计学意义(P<0.05)。结论丁苯酞具有缓解动脉粥样硬化脑梗死引起的神经元凋亡作用,并可促进PI3K/Akt通路和血管生成。

Objective To study the effect of butylphthalide on neural function in acute atheroscle-rotic cerebral infarction rats.Methods Forty-two SPF-SD rats were randomly divided into con-trol group,model group and butylphthalide group(14 in each group).The carotid artery in ani-mals of control group fed on a normal food was exposed but not ligated.After the atherosclerosis model and cerebral infarction model were established for model group and butylphthalide group,the animals in butylphthalide group were given butylphthalide while those in control group and model group were given the same volume of normal saline by intravenous injection.The neural function of animals in different groups was assessed according to their mNSS and water maze test.The expressions of neuron-specific enolase(NSE),endothelin 1,phosphatidylinositol 3 ki-nase(PI3K),protein kinase B(Akt),VEGF mRNA and protein were detected.Results The mNSS,apoptosis index,expression levls of NSE and endothelin 1 were significantly higher and the cerebal infarction volume was significantly larger while the number of involved blood vessels was significantly smaller and the expression levels of PI3K,Akt and VEGF mRNA and protein were significantly lower in model group than in control group(P<0.05).The mNSS,apoptosis index,expression levls of NSE and endothelin 1 were significantly lower and the cerebal infarction vol-ume was significantly smaller in butylphthalide group than in model group(5.86±1.02 vs 12.85±2.16,14.38%±2.43%vs 36.45%±4.78%,20.43%±2.56%vs 46.75%±3.72%,11.24±1.53μg/L vs 15.86±2.24μg/L,40.35±4.74μg/L vs 51.17±6.21μg/L,P<0.05)while the number of involved blood vessels was significantly greater and the expression levels of PI3K,Akt and VEGF mRNA and protein were significantly higher in butylphthalide group than in model group(P<0.05).Conclusion Butylphthalide can alleviate the neuronal apoptosis induced by atherosclerotic cerebral infarction,upregulate the expression of VEGF mRNA and protein,and pronote the angiogenesis through the PI3K/Akt pathway.