论文部分内容阅读
目的研究G蛋白耦联受体43(GPR43)在哮喘小鼠肺组织内的表达,同时探讨地塞米松对GPR43表达的影响。方法 30只BALB/C6小鼠随机分为对照组、哮喘组、地塞米松组,每组10只;卵清白蛋白(OVA)致敏和激发建立哮喘小鼠模型;肺泡灌洗液(BALF)细胞计数;HE染色观察各组气道炎症发生及气道结构改变情况;RT-PCR测定各组小鼠肺组织GPR43mRNA的表达变化;免疫组化观察肺中GPR43的表达及定位。结果哮喘组BALF嗜酸性粒细胞(EOS)与对照组相比明显增高,地塞米松组明显低于哮喘组(P<0.01);HE染色提示哮喘组气道上皮出现EOS等大量炎性细胞浸润,管壁厚度较对照组明显增加(P<0.01);RT-PCR结果提示GPR43受体mRNA的表达量在哮喘组最低,与对照、地塞米松组相比有统计学差异(P<0.01);免疫组化图像分析提示GPR43蛋白表达哮喘组明显降低,与对照组、地塞米松组相比均有显著性差异(P<0.01)。结论哮喘小鼠肺组织中GPR43表达下降,地塞米松能部分上调其表达,从而减轻气道炎症反应。
Objective To investigate the expression of G protein-coupled receptor 43 (GPR43) in the lung tissue of asthmatic mice and the effect of dexamethasone on GPR43 expression. Methods Thirty BALB / c mice were randomly divided into control group, asthma group and dexamethasone group, with 10 mice in each group. Asthmatic mice were sensitized and challenged with ovalbumin (OVA) Count; HE staining was used to observe the changes of airway inflammation and airway structure in each group; RT-PCR was used to detect the expression of GPR43mRNA in lung tissue of each group; immunohistochemistry was used to observe the expression and localization of GPR43 in lung. Results Compared with the control group, the eosinophils in BALF of asthmatic group were significantly higher than that of the control group (P <0.01), and the number of EOS in the asthmatic group was significantly higher than that of the asthma group (P <0.01). The results of RT-PCR indicated that the expression of GPR43 receptor mRNA in the asthma group was the lowest (P <0.01), compared with the control group and the dexamethasone group Immunohistochemical analysis showed that GPR43 protein expression in asthma group was significantly lower than that in control group and dexamethasone group (P <0.01). Conclusion The expression of GPR43 in the lung tissue of asthmatic mice decreased, and dexamethasone partially up-regulated the expression of GPR43, thereby reducing the airway inflammatory response.