HMGB1/NF-κB通路在脑梗死治疗中的调控研究  

The underling regulation mechanisms of HMGB1/NF-κB pathway activity in ischemia-reperfusion injury

作　　者：王力娜[1] 刘莹[1] 季辉[1] 苗江永[1] 张祥建[1] Wang Lina;Liu Ying;Ji Hui;Miao Jiangyong;Zhang Xiangjian(Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)

机构地区：[1]河北医科大学第二医院神经内科,石家庄050000

出　　处：《脑与神经疾病杂志》2021年第6期335-340,共6页Journal of Brain and Nervous Diseases

基　　金：国家自然科学基金会项目(81571292)。

摘　　要：目的探讨脑梗死后HMGB1/NF-κB信号通路的活性变化及丹参酮ⅡA发挥调控作用的具体机制。方法应用改良线栓法制备大脑中动脉脑梗死模型,健康雄性SD大鼠随机分为4个亚组:正常组、缺血组和给药组(分别为丹参酮ⅡA 10 mg·kg-1,丹参酮ⅡA 20mg·kg-1)。实验采用免疫组织化学、Western blot和RT-PCR等方法观察HMGB1、NF-κB的表达变化,以及丹参酮ⅡA在脑梗死后继发缺血损伤中的神经保护作用及其对HMGB1/NF-κB信号转导通路的作用。结果HMGB1在脑缺血损伤过程中表达可上调,缺血3 h开始上升,于24 h表达至高峰,缺血48h后逐渐下降,可持续至14d。给予丹参酮ⅡA治疗后可以有效减轻神经功能以及组织的损伤,其作用可能与其下调HMGB1、NF-κB表达,抑制炎症反应有关。结论HMB1/NF-κB通路参与了丹参酮ⅡA的脑保护作用,为其临床进一步应用提供了理论基础。Objective This study is to evaluate HMGB1/NF-κB pathway activity in ischemia injury and explore the underling regulation mechanisms of tanshinoneⅡA.Methods Male Sprague-Dawley(SD)rats were subjected to pMCAO.TanshinoneⅡA was systemically administered to explore the effect on HMGB1 and NF-κB at 24h after cerebral ischemia by immunohistochemistry,Western blot and qRT-PCR.The neurological deficits,brain water content and infarct volume were measured.Results The expressions of HMGB1 increased at 3 h,reached to maximum at 24 h,decreased lightly at 48 h,in both of imunohistochemical staining,Western blot and RT-PCR.TanshinoneⅡA dramatically down-regulated HMGB1 and NF-κB,alleviated the neurological deficits,brain water content and infarct volume.Conclusion HMGB1/NF-κB pathway is involved in the cerebral protective effects of TanshinoneⅡA,providing a theoretical basis for its clinical application for cerebral ischemic therapies.

关 键 词：脑缺血 高迁移率族蛋B1 核因子-ΚB 丹参酮ⅡA 

分 类 号：R743.34[医药卫生—神经病学与精神病学]