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中国充血性心力衰竭患者血清中抗β(1)-肾上腺素能受体自身抗体呈阳性,可降低小鼠心肌细胞的内向整流钾电流(I(ss)) 。

Serum positive for the autoantibody against the β(1)-adrenoceptor from Chinese patients with congestive heart failure decreases I(ss) in mouse cardiac myocytes.

作者信息

Wang Yuan-yuan, Ma Zhi-Yong, Li Xiao-Dong, Wang Jian-chun, Zhang Wei, Li Li, Zhang Yun

机构信息

Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Jinan 250012, China.

出版信息

Clin Dev Immunol. 2011;2011:143517. doi: 10.1155/2011/143517. Epub 2011 Jun 7.

DOI:10.1155/2011/143517
PMID:21716722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3119415/
Abstract

Autoantibodies targeting the β(1)-adrenergic receptor (AAB-β(1)) display agonist-like effects, which may have a pathogenic role in the progression of heart failure. Here, we used the electrophysiological recordings to explore the effects of AAB-β(1)-positive serum from Chinese patients with heart failure on the activity of the peak transient outward potassium current (I(to)) and the end 50 ms steady-state potassium current (I(ss)) in mouse cardiac myocytes. We found that the AAB-β(1)-positive serum had no effect on the activity of I(to), but it produced a decrease in the currents of I(ss). A low concentration of positive serum (1/100) had a small inhibitory effect on I(ss). However, positive serum at 1 : 10, 1 : 20, and 1 : 50 significantly decreased I(ss). The concentration-dependence analysis showed that the EC(50) of AAB-β(1)-positive serum was 1/60.24 and its nH was 2.86. It indicated that the AAB-β(1) could inhibit I(ss) in mouse cardiomyocyte in a concentration-dependent manner.

摘要

靶向β(1)-肾上腺素能受体的自身抗体(AAB-β(1))表现出激动剂样效应,这可能在心力衰竭进展中具有致病作用。在此,我们使用电生理记录来探究中国心力衰竭患者的AAB-β(1)阳性血清对小鼠心肌细胞中瞬时外向钾电流峰值(I(to))和50毫秒末稳态钾电流(I(ss))活性的影响。我们发现,AAB-β(1)阳性血清对I(to)活性无影响,但会使I(ss)电流降低。低浓度阳性血清(1/100)对I(ss)有轻微抑制作用。然而,1:10、1:20和1:50的阳性血清显著降低了I(ss)。浓度依赖性分析表明,AAB-β(1)阳性血清的半数有效浓度(EC(50))为1/60.24,其Hill系数(nH)为2.86。这表明AAB-β(1)可在小鼠心肌细胞中以浓度依赖性方式抑制I(ss)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/4c09d2cf12a6/CDI2011-143517.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/2831335924cc/CDI2011-143517.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/f7b8e4bf0126/CDI2011-143517.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/52eb4ca40499/CDI2011-143517.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/4c09d2cf12a6/CDI2011-143517.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/2831335924cc/CDI2011-143517.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/f7b8e4bf0126/CDI2011-143517.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/52eb4ca40499/CDI2011-143517.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce38/3119415/4c09d2cf12a6/CDI2011-143517.004.jpg

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