色甘酸钠和壁内神经节对卵清蛋白诱发支气管哮喘大鼠支气管中 TNFR1 基因表达的影响

L. E. Blazhevich, Olga E. Smirnova, V. Kirilina, P. M. Maslyukov
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摘要

本文的目的是研究卵清蛋白诱导的支气管哮喘大鼠支气管中 TNFR1 基因的表达,同时考虑到支气管内变态反应神经节和色甘酸钠对肥大细胞膜的稳定作用。本文中的基因表达是指支气管组织中 mRNA 的积累。TNFR1 基因和受体的表达在过敏性哮喘的发病过程中起着重要作用。因此,本文选择 TNFR1 基因进行分析。材料与方法使用实时聚合酶链反应对 Wistar 大鼠的支气管样本进行研究。实验中,取有神经节的支气管(分叉区)和无神经节的支气管(直切片)。材料取自 7 组大鼠:卵清蛋白诱导的支气管哮喘(6 组)和对照组(1 组)。对 3 组模拟哮喘大鼠使用了色甘酸钠肥大细胞稳定剂。结果显示研究发现,在发生支气管哮喘的大鼠中,编码 TNFR1 的 mRNA 表达量增加。在有神经节的支气管样本中,TNFR1基因的表达高于无神经节的支气管样本。在色甘酸钠的影响下,TNFR1 基因表达下降。根据所得结果,研究人员认为肥大细胞和神经节内神经元对 TNFR1 基因表达有相当明显的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Sodium Cromoglycate and Intramural Ganglia on TNFR1 Gene Expression in the Bronchi of Rats with Ovalbumin-Induced Bronchial Asthma
The purpose of this article was to study TNFR1 gene expression in the bronchi of rats with ovalbumininduced bronchial asthma, taking into account intramural metasympathetic ganglia and the stabilization of mast cell membranes with sodium cromoglycate. In this paper, gene expression refers to the accumulation of mRNA in bronchial tissues. Expression of the TNFR1 gene and receptor plays an important role in the development of allergic asthma. For this reason, the TNFR1 gene was chosen for the analysis. Materials and methods. Bronchial samples from Wistar rats were studied using real-time polymerase chain reaction. For experiments, bronchi with ganglia (in the bifurcation area) and bronchi without ganglia (straight sections) were taken. The material was collected from 7 groups of rats: with ovalbumin-induced bronchial asthma (6 groups) and control animals (1 group). Mast cell stabilizer sodium cromoglycate was used to treat 3 groups of rats with simulated asthma. Results. It was found that the expression of mRNA encoding TNFR1 increases in rats developing bronchial asthma. In bronchial samples with ganglia, TNFR1 gene expression was higher than in bronchial preparations without ganglia. Under the influence of sodium cromoglycate, TNFR1 gene expression decreased. Based on the results obtained, it was suggested that mast cells and neurons of the intramural ganglion have a rather pronounced effect on TNFR1 gene expression.
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