摘要
目的采用大鼠局灶性脑缺血模型,观察TWEAK、NF-κB的表达及氧化苦参碱的干预作用。方法 SD大鼠随机分为4组:正常组、缺血组、和给药组(氧化苦参碱60,120mg·kg^-1)。应用线栓法建立局灶性脑缺血模型,术后6 h,24 h,48 h,72 h、用免疫组织化学方法、Western blot及RT-PCR检测缺血周围区TWEAK和NF-κB表达的变化。结果免疫组化、Western blot及RT-PCR显示TWEAK的表达水平在脑梗死后6 h内上升,48 h达高峰,72 h逐渐下降。氧化苦参碱120mg·kg^-1能改善大鼠缺血后神经功能评分、减少梗死体积,显著降低缺血后TWEAK和NF-κB表达量的升高。结论实验证实了TWEAK的表达参与了脑缺血后继发性损伤,氧化苦参碱可通过下调TWEAK、NF-κB表达,减轻缺血后脑损伤。
objective To observe the expression of TWEAK and NF-κB in rat brain after focal cerebral ischemia and the effect of oxymatrine on the expression.Methods SD rats were divided randomly into normal group,ischemia group and treatment group(oxymatrine 60,120 mg·kg^-1).A model of the middle cerebral artery occlusion in rats was performed with the intraluminal filament occlusion.6 h,24 h,48 h,72 h after operation,immunohistochemical staining,Western blot and RT-PCR were respectively used to detect the expression of TWEAK and NF-κB around ischemic area.Results The expression of TWEAK increased at 6 h,reached to maximum at48 h,decreased lightly at 72 h,in both of immunohistochemical staining,Western blot and RT-PCR.Oxymatrine120 mg·kg^-1 can improve the score of nerve function after ischemia and reduce the volume of infarction.TWEAK and NF-κB protein expression demonstrated statistically significant decrease in oxymatrine at dose of 120 mg·kg^-1,compared with ischemia group.The same trends appeared in RT-PCR product.Conclusion The present results confirmed that TWEAK was involved in cerebral injury following cerebral ischemia.Oxymatrine can reduce cerebral injury after ischemia by down regulate the expression of TWEAK and NF-κB.
作者
刘莹
王力娜
崔丽丽
张祥建
季辉
LiuYing;Wang lina;Cui Lili;Zhang Xiangjian;Ji Hui(Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)
出处
《脑与神经疾病杂志》
2020年第3期137-143,共7页
Journal of Brain and Nervous Diseases
基金
国家自然科学基金会项目（81571292）
河北省卫计委科技课题（20170098）
