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黄连素预处理对大鼠心肌缺血再灌注损伤的保护作用
引用本文:张童,.黄连素预处理对大鼠心肌缺血再灌注损伤的保护作用[J].四川医学,2018,39(4):393-396.
作者姓名:张童  
作者单位:成都医学院第二附属医院,核工业四一六医院
摘    要:目的探讨黄连素(Berberine,BBR)预处理对大鼠心肌缺血再灌注损伤的作用及其机制。方法建立大鼠心肌缺血再灌注损伤模型。30只雄性SD大鼠随机均分为假手术组(Sham)、心肌缺血/再灌注损伤组(IRI)和黄连素组(BBR)。检测各组大鼠心肌功能、病理形态、JAK2、STAT3、p-JAK2、p-STAT3、p-NF-KB、NF-KB、白介素-6(IL-6)、白介素1(IL-1β)和肿瘤坏死因子-α(TNF-α)的表达。结果与Sham组相比,IRI组心肌失功,心肌病理改变,p-JAK2,p-STAT3,p-NF-KB,IL-6,IL-1和TNF-表达明显增加,而JAK2,STAT3和NF-KB表达无明显差异。与IRI组相比,BBR组IRI组心肌失功,心肌病理改变,p-JAK2,p-STAT3,p-NF-KB,IL-6,IL-1和TNF-表达明显减少,而JAK2,STAT3和NF-KB表达依然无明显差异。结论黄连素预处理可通过抑制JAK2/STAT3/NF-KB信号通路激活而减少炎症反应,从而减轻心肌缺血再灌注损伤。

关 键 词:黄连素    心肌缺血再灌注损伤    炎症    JAK2/STAT3/NF-KB

Berberine Pretreatment Ameliorates Myocardial Ischemia Reperfusion Injury
Zhang Tong.Berberine Pretreatment Ameliorates Myocardial Ischemia Reperfusion Injury[J].Sichuan Medical Journal,2018,39(4):393-396.
Authors:Zhang Tong
Institution:Nuclear Industry 416 Hospital
Abstract:Objective To investigate potential protection and mechanism of Berberine in myocardial ischemia reperfusion injury.Methods Constructing the model of myocardial ischemia reperfusion injury.30 male SD rats were randomly equally divided into Sham group( Sham),myocardial ischemia reperfusion injury group( IRI),and Berbrine pretreatment group( BBR).The cardial function,histology of myocardial,expression of JAK2,STAT3,p-JAK2,p-STAT3,p-NF-KB,NF-KB,IL-6,IL-1 and TNF-in the rats of all groups were exanimed.Results Compared with the Sham group,the myocardial dysfuction,the pathological of heart and the expression of p-JAK2,p-STAT3,p-NF-KB,IL-6,IL-1 and TNF-in IRI group were significantly increased with no difference in the expression of JAK2,STAT3 and NF-KB.Compared with the IRI group,the myocardial dysfuction,the pathological of heart and the expression of p-JAK2,p-STAT3,p-NF-KB,IL-6,IL-1 and TNF-in IRI group were significantly decreased with still no difference in the expression of JAK2,STAT3 and NF-KB. Conclusion Berberin pretreatment protect myocardial ischemia reperfusion injury from inflammation by suppressing the activation of JAK2/STATA3/NF-KB signal pathway
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