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E-prostanoid receptor distribution in airway smooth muscle cells of a rat model of asthma

机译:E-前列腺素受体在哮喘大鼠模型气道平滑肌细胞中的分布

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Airway remodeling is a main pathological characteristic of asthma, and strongly associated with migration and proliferation of airway smooth muscle cells. E-prostanoid (EP) receptor can regulate airway remodeling. This study established a rat model of asthma and evaluated EP changes in airway smooth muscle cells under the asthmatic state so as to provide theoretical evidence for developing EP drugs to treat airway remodeling in asthma. A total of 20 clean Sprague-Dawley rats were randomly assigned to asthma group and control group. 28 days later, they were sacrificed for histological examination. Airway smooth muscle cells were isolated, cultured and measured using quantitative fluorescent PCR. Histopathological examination revealed that rat models of asthma were in accordance with the manifestations of asthmatic airway remodeling. After reverse transcription, real-time quantitative fluorescent PCR was performed using miRNA Q-PCR diagnostic kit. GAPDH was considered the internal reference. Relative expressions of E-prostanoid 1-4 (EP1-4) (2~(-△△~(Ct))) in the control and asthma groups were respectively as follows: EP1: 4.35±0.18, 6.55±1.21; EP2: 3.64±0.12, 1.35±1.06; EP3: 4.59±1.14, 5.89±1.74; EP4: 2.89±1.85, 1.69±0.44. EP2/4 significantly decreased, but EP1 significantly increased in the asthma group (P < 0.01). These results suggested that the reduced EP2/4 and increased EP1 expressions in airway smooth muscle cells of rat models of asthma were probably important factors for asthmatic airway remodeling.
机译:气道重塑是哮喘的主要病理特征,与气道平滑肌细胞的迁移和增殖密切相关。 E-前列腺素(EP)受体可以调节气道重塑。这项研究建立了哮喘的大鼠模型,并评估了哮喘状态下气道平滑肌细胞中EP的变化,从而为开发用于治疗哮喘气道重塑的EP药物提供了理论依据。将总共​​20只干净的Sprague-Dawley大鼠随机分为哮喘组和对照组。 28天后,将其处死以进行组织学检查。分离,培养并使用定量荧光PCR测量气道平滑肌细胞。组织病理学检查显示,大鼠哮喘模型符合哮喘气道重塑的表现。逆转录后,使用miRNA Q-PCR诊断试剂盒进行实时定量荧光PCR。 GAPDH被视为内部参考。对照组和哮喘组中E-前列腺素1-4(EP1-4)(2〜(-△△〜(Ct)))的相对表达分别为:EP1:4.35±0.18,6.55±1.21; EP2:3.64±0.12、1.35±1.06; EP3:4.59±1.14、5.89±1.74; EP4:2.89±1.85,1.69±0.44。在哮喘组中,EP2 / 4显着降低,但EP1显着升高(P <0.01)。这些结果表明,哮喘模型的气道平滑肌细胞中EP2 / 4的减少和EP1表达的增加可能是哮喘气道重塑的重要因素。

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