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原发性高血压患者中抗α1肾上腺素受体自身抗体激活大鼠主动脉平滑肌细胞内NF-κB
引用本文:孙艳香,袁勇,冯力,廖玉华,朱峰.原发性高血压患者中抗α1肾上腺素受体自身抗体激活大鼠主动脉平滑肌细胞内NF-κB[J].中国病理生理杂志,2014,30(3):514-517.
作者姓名:孙艳香  袁勇  冯力  廖玉华  朱峰
作者单位:1中山大学附属中山医院心血管内科, 广东 中山 528400; 2华中科技大学同济医学院附属协和医院心血管内科, 湖北 武汉 430022
基金项目:国家自然科学基金资助项目(No.C03030201); 中国博士后科学基金资助项目(No. 20100470982)
摘    要: 目的:探讨高血压患者血清中抗α1肾上腺素受体自身抗体(autoantibodies against α1-adrenergic receptor, α1-AAs)拟去甲肾上腺素的激动样效应及胞内信号分子活化机制。方法:培养大鼠主动脉平滑肌细胞。将收集的原发性高血压病人血清进行免疫亲和层析法纯化,ELISA检测其滴度后以1∶80刺激细胞,并设立不同的处理组。将α1-AAs刺激大鼠主动脉平滑肌细胞后,经Western blotting及免疫荧光方法分析胞内核因子κB (nuclear factor κB, NF-κB) 信号分子激活及表达状况。结果:Western bltting显示α1-AAs刺激组中胞内核因子NF-κB (p50)表达较空白对照组明显增强,且可被α1受体阻滞剂哌唑嗪和NF-κB拮抗剂PDTC明显抑制(P<0.05)。免疫荧光实验中,α1-AAs组荧光强度显著高于空白对照组和α1-AAs+哌唑嗪组(P<0.01)。结论:高血压患者血清中α1-AAs能够致大鼠主动脉平滑肌细胞NF-κB活化。

关 键 词:高血压  α1肾上腺素受体  自身抗体  NF-κB  
收稿时间:2013-09-18

Activation of NF-κB in rat vascular smooth muscle cells by autoantibodies against α1-adrenergic receptor from hypertensive patients
SUN Yan-xiang,YUAN Yong,FENG Li,LIAO Yu-hua,ZHU Feng.Activation of NF-κB in rat vascular smooth muscle cells by autoantibodies against α1-adrenergic receptor from hypertensive patients[J].Chinese Journal of Pathophysiology,2014,30(3):514-517.
Authors:SUN Yan-xiang  YUAN Yong  FENG Li  LIAO Yu-hua  ZHU Feng
Institution:1Department of Cardiovascular Medicine, Zhongshan Hospital, Sun Yat-sen University, Zhongshan 528400, China; 2Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Abstract:AIM:To study the effects of autoantibodies against α1-adrenergic receptor (α1-AAs) isolated from the hypertensive patients, which showed the agonist-like activity similar to norepinephrine, on the signal mechanism of vascular smooth muscle cells (VSMCs) isolated from rat thoracic aorta. METHODS:Rat VSMCs were cultured and identified. The serum of hypertensive patients was purified by immunoaffinity chromatography. The autoantibodies were detected by ELISA and used to activate the cells with the titer of 1∶80. The total protein  was extracted and the expression of NF-κB in different treatment groups was detected by Western blotting. Meanwhile, the activation of NF-κB in the nucleus was analyzed by immunofluorescence method. RESULTS:The expression of NF-κB in VSMCs was obviously higher in α1-AAs group than that in control group. Meanwhile, the expression of NF-κB was inhibited by prasozin and PDTC. The autoantibodies caused a significant increase in NF-κB expression in the nucleus. The fluorescence intensity in α1-AAs group was high than that in control group and α1-AAs+prasozin group (P<0.01). CONCLUSION:The α1-AAs from hypertensive patients increase NF-κB expression in rat VSMCs.
Keywords:Hypertension  &alpha  1-adrenergic receptors  Autoantibody  NF-kappa B
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