| 于 嘉,金 鑫,孙 鹏,陈 玲,方 伟.丁苯酞对脑梗死模型大鼠血清及脑组织突触素及突触后致密物-95表达的影响[J].现代生物医学进展英文版,2022,(9):1620-1624. |
| 丁苯酞对脑梗死模型大鼠血清及脑组织突触素及突触后致密物-95表达的影响 |
| Effects of Butylphthalide on the Expression of Synaptophysin and Postsynaptic Density-95 in Serum and Brain Tissues of Rats with Cerebral Infarction |
| Received:September 03, 2021 Revised:September 26, 2021 |
| DOI：10.13241/j.cnki.pmb.2022.09.004 |
| 中文关键词: 丁苯酞 脑梗死 突触素 突触后致密物-95 阿司匹林 改良神经功能评分 |
| 英文关键词: Butylphthalide Cerebral infarction Synaptophysin Postsynaptic compact-95 Aspirin Modified neurological score |
| 基金项目:陕西省科技创新工程基金资助项目（2017KTCL03-05） |
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| 中文摘要: |
| 摘要 目的：探讨丁苯酞对脑梗死模型大鼠血清及脑组织突触素及突触后致密物（postsynaptic density，PSD）-95表达的影响。方法：将建模成功的大鼠随机平分为三组-丁苯酞组、阿司匹林组与模型组各18只。三组分别给予腹腔注射丁苯酞注射液20 mg/kg+阿司匹林20 mg/kg、阿司匹林20 mg/kg与等体积的生理盐水，1次/d，检测血清及脑组织突触素及PSD-95表达变化情况。结果：（1）治疗第7 d与治疗第14 d后，丁苯酞组和阿司匹林组大鼠改良神经功能评分（Modified neurological severity scores，mNSS）均显著低于模型组（P<0.05），丁苯酞组低于阿司匹林组（P<0.05）；（2）治疗第7 d与治疗第14 d，丁苯酞组、阿司匹林组大鼠的脑梗死体积百分比均显著低于模型组（P<0.05），丁苯酞组低于阿司匹林组（P<0.05）；（3）治疗第7 d与治疗第14 d，丁苯酞组、阿司匹林组大鼠血清突触素及PSD-95表达水平均显著高于模型组（P<0.05），丁苯酞组高于阿司匹林组（P<0.05）；（4）治疗第7 d与治疗第14 d后，丁苯酞组、阿司匹林组大鼠大脑组织突触素及PSD-95蛋白相对表达水平均显著高于模型组（P<0.05），丁苯酞组高于阿司匹林组（P<0.05）。结论：丁苯酞在脑梗死模型大鼠的应用可促进大鼠血清及脑组织突触素及PSD-95的表达，并减小脑梗死面积，因而有利于大鼠的神经功能的恢复。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of butylphthalide on the expression of synaptophysin and postsynaptic density (PSD)-95 in serum and brain tissue of rats with cerebral infarction. Methods: The successfully modeled rats of cerebral infarction were equally randomly divided into three groups-butylphthalide group, aspirin group and model group. The three groups were given intraperitoneal injection of butylphthalide injection 20 mg/kg+ aspirin 20 mg/kg, aspirin 20 mg/kg and equal volume of saline, once daily, and the changes in the expression of synaptophysin and PSD-95 in serum and brain tissue were detected. Results: (1) On the 7th day and the 14th day after treatment, the mNSS of the rats in the butylphthalide group and the aspirin group were significantly lower than those in the model group (P<0.05), and the butylphthalide group was lower than the aspirin group (P<0.05); (2) On the 7th day and the 14th day after treatment, the percentage of cerebral infarction volume of rats in the butylphthalide group and the aspirin group was significantly lower than that of the model group(P<0.05), and the butylphthalide group was lower than the aspirin group(P<0.05); (3) On the 7th day of treatment and the 14th day of treatment, the expression levels of serum synaptophysin and PSD-95 in the butylphthalide group and aspirin group were significantly higher than those in the model group(P<0.05), and the butylphthalide group was higher than the aspirin group(P<0.05); (4) The relative expression levels of synaptophysin and PSD-95 protein in the brain tissue of the rats in the butylphthalide group and the aspirin group were significantly higher than those in the model group on the 7th day and the 14th day after treatment (P<0.05), and the butylphthalide group was higher than the aspirin group (P<0.05). Conclusion: The application of butylphthalide in cerebral infarction model rats can promote the expression of synaptophysin and PSD-95 in rat serum and brain tissue, and reduce the area of cerebral infarction, which is conducive to the recovery of neurological function in rats. |
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