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Biological characteristics of tracheal smooth muscle cells regulated by NK-1R in asthmatic rat with airway remodeling

机译:NK-1R调节哮喘气道重塑大鼠气管平滑肌细胞的生物学特性。

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摘要

This study aims to investigate the biological characteristic changes of infant rat tracheal smooth muscle cells in asthma airway remodeling and the impact of NK-1R on the mechanism. Ovalbumin (OVA) was used to excited juvenile SD rats by 8 w. Immunofluorescence, MTT assay, transwell chambers, real time quantitative PCR, Western blot and other methods were used to observe the proliferation, migration, synthesis and secretion changes of infant airway remodeling in rat tracheal smooth muscle cell and the Neurokinin 1 receptor (NK-1R) expression. 1. NK-1R mRNA, protein expression of airway smooth muscle cell (ASMC) of each asthma group were higher than that of the control group, especially the asthma 8 w group had highest expression (P<0.01). 2. The average A value of 8 w asthma group measured by MTT method were significantly higher than that of the control group (P<0.05), WIN62577 10-8 mol/L group had the strongest inhibition of ASMC proliferation (P<0.01). 3. The number of cell migration in the asthma group significantly increased than that in the control group. The number of migrating cells in the NK-1R antagonist group significantly reduced compared with the asthma 8 w group (P<0.05). 4. The average gray value of type III collagen in each asthma group were higher than that of the control group, and the asthma 8 w group had the highest (P<0.01). After NK-1R blocking, the average gray value of type III collagen was significantly lower (P<0.05). ASMC proliferation, migration, synthesis and secretion function increased in the airway remodeling group, and NK-1R played an important role.
机译:本研究旨在探讨婴儿气管平滑肌细胞在哮喘气道重塑中的生物学特性变化以及NK-1R对其机制的影响。用卵清蛋白(OVA)激发SD大鼠8 w。免疫荧光,MTT法,穿孔室,实时定量PCR,Western blot等方法观察婴儿气管重塑在大鼠气管平滑肌细胞和神经激肽1受体(NK-1R)的增殖,迁移,合成和分泌变化。 )表达。 1.各哮喘组气道平滑肌细胞NK-1R mRNA,蛋白表达均高于对照组,其中哮喘8w组表达最高(P <0.01)。 2. MTT法测定8 w哮喘组的平均A值明显高于对照组(P <0.05),WIN62577 10 -8 mol / L组对哮喘的抑制作用最强。 ASMC增殖(P <0.01)。 3.哮喘组的细胞迁移数量比对照组明显增加。与哮喘8 w组相比,NK-1R拮抗剂组的迁移细胞数量显着减少(P <0.05)。 4.哮喘各组中Ⅲ型胶原蛋白的平均灰度值均高于对照组,且哮喘8 w组最高(P <0.01)。 NK-1R阻断后,III型胶原蛋白的平均灰度值显着降低(P <0.05)。在气道重塑组中,ASMC的增殖,迁移,合成和分泌功能增强,而NK-1R发挥了重要作用。

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