葛根素预处理抑制NF-κB p65蛋白表达减轻在体大鼠心肌缺血再灌注损伤

Preconditioning of puerarin reduce the myocardial ischemiareperfusion injury by inhibiting the transcription of NF-κB

目的:观察葛根素预处理在体大鼠心肌缺血再灌注损伤(I/R)时是否抑制核因子(NF)-κBp65蛋白表达并减少循环和心脏局部肾素-血管紧张素系统(RAS)水平。方法:建立在体大鼠心肌I/R模型,设立假手术组、I/R组和葛根素预处理组。以氯化四唑染色法测定各组心肌梗死面积;测定心肌酶学水平和光镜改变;应用免疫组织化学法定性检测心肌组织NF-κBp65蛋白活化的细胞定位;以酶联免疫吸附法(ELISA)检测NF-κBp65蛋白及其DNA结合活性;以放射免疫分析法测定血浆和心肌组织血管紧张素Ⅱ(AngⅡ)含量。结果:与I/R组比较,葛根素预处理组心肌梗死面积明显缩小,心肌酶学水平浓度明显降低(P均<0.05);血浆和心肌组织AngⅡ含量显著降低及NF-κBp65的蛋白活性明显受抑(P均<0.05)。结论:葛根素预处理可经抑制NF-κBp65蛋白表达并减少循环和心脏局部RAS水平,从而减轻心肌缺血再灌注损伤。

Objective： To investigate whether preconditioning of puerarin could inhibit both NF-κB 65protein activation and circulatory or cardiac local RAS in rat with myocardial ischemia/reperfusion injury （I/R）. Methods： Thirty- six healthy male SD rats were randomly divided into sham-operated group （sham group）, I/R model group and puerarin preconditioning group （n= 12）. Myocardial infarct size was measured hy TTC. Serum myocardial enzymes were measured and light microscopic study was performed; the localization of NF-κB was detected by immunohistochemistry and the quantitation of activated NF-κB was detected by enzyme-linked immunosorbent assay （ELISA） ; the plasma and myocardium Ang Ⅱ content was measured by radioimmunoassay method. Results： Compared with I/R group, infarction area was significant smaller in the puerarin pretreatment group （P〈0.05） and myocardial enzyme levels were significantly lower （P〈0.05 all）. The Ang Ⅱ content in circulation and cardiac myocyte significantly decreased （P〈0. 05 all）. Conclusion： Preconditioning of puerarin could reduce I/R by inhibiting NF-κBp65 protein activity and reducing the levels of Ang Ⅱboth circulation and local heart.