丁苯酞对缺血性脑卒中大鼠脑组织NF-κB p65、IL-6、TNF-α表达的影响  

Effects of butylphthalide on expression of serum NF-κB p65,IL-6 and TNF-α in rats with cerebral ischemic stroke

作　　者：张晓璇[1] 朱江[1] 李佳佳[1] 焦光美[1] 单海雷 赵亮[1] 窦志杰[1] ZHANG Xiao-Xuan;ZHU Jiang;LI Jia-Jia;JIAO Guang-Mei;SHAN Hai-Lei;ZHAO Liang;DOU Zhi-Jie(Department of Neurology,Affiliated Hospital of Chengde Medical University,Chengde 067000,China)

机构地区：[1]承德医学院附属医院神经内科

出　　处：《中国免疫学杂志》2019年第15期1825-1828,1834,共5页Chinese Journal of Immunology

基　　金：河北省卫计委医学科学项目(20181160);承德市科技局项目(201804A081)资助

摘　　要：目的:观察丁苯酞对缺血性脑卒中大鼠脑组织NF-κB p65、IL-6、TNF-α表达的影响,阐明其作用机制。方法:将50只大鼠随机分为假手术组、模型组、丁苯酞低、中、高剂量组(剂量分别为20、40、60 mg/kg)。模型组、丁苯酞低、中、高剂量采用右侧大脑中动脉阻塞法建立大鼠缺血性脑卒中模型,假手术组不进行栓线操作。采用Bederson法对大鼠进行神经功能评分,采用TTC染色法观察大鼠脑梗死体积,Western blot检测大鼠脑组织NF-κB p65蛋白表达水平,采用免疫荧光方法观察NF-κB p65入核情况。酶联免疫吸附检测大鼠脑组织IL-6、TNF-α水平。结果:与假手术组比较,模型组大鼠神经功能评分和脑梗死体积显著增加,脑组织NF-κB p65蛋白表达水平显著升高,NF-κB p65入核显著增加,IL-6、TNF-α水平显著增加( P <0.05)。与模型组比较,丁苯酞低、中、高剂量组神经功能评分和脑梗死体积显著减少,脑组织NF-κB p65蛋白表达水平显著降低,NF-κB p65入核显著减少,IL-6、TNF-α水平显著降低( P <0.05)。结论:丁苯酞对缺血性脑卒中有保护作用,其机制与抑制脑组织NF-κB p65活化,降低脑组织炎性因子IL-6、TNF-α水平有关。Objective: To observe the effect of butylphthalide on the expression of brain NF-κB p65,IL-6 and TNF-α in rats with cerebral ischemic stroke,and elucidate its mechanism. Methods: Fifty rats were randomly divided into sham operation group,model group,butylphthalide low,medium and high doses group(20 mg/kg,40 mg/kg,60 mg/kg).The model of ischemic stroke in rats was established by right middle cerebral artery occlusion while the sham operation group did not perform suture operation.Bederson method was used to detected neurological deficit scores in rats.The volume of cerebral infarction was observed by TTC staining.Western blot was used to detect protein expression of NF-κB p65 in rat brain tissue.The levels of IL-6 and TNF-α were detected by ELISA.Nuclear displacement of NF-κB p65 was observed by immunofluorescence method. Results: Compared with sham operation group,the neurological deficit scores and cerebral infarction volume of the model group significantly increased,the protein expression level of brain tissue NF-κB p65 significantly increased,nuclear displacement of NF-κB p65 produced a significant increase,and IL-6 and TNF-α level significantly increased ( P <0.05).Compared with model group,the neurological deficit scores and cerebral infarction volume of butylphthalide low,medium and high dose group were significantly reduced,the expression level of NF-κB p65 protein in brain tissue was significantly reduced,nuclear displacement of NF-κB p65 decreased significantly,and the level of IL-6 and TNF-α were significantly reduced ( P <0.05). Conclusion: Butylphthalide has a protective effect on ischemic stroke,and its mechanism is related to inhibiting the activity of NF-κB p65 and reducing the levels of inflammatory factors IL-6 and TNF-α in brain tissue.

关 键 词：缺血性脑卒中 丁苯酞 NF-ΚB P65 IL-6 TNF-α 

分 类 号：R743.3[医药卫生—神经病学与精神病学]