| 摘要: |
| 目的：观察肝郁型哮喘小鼠模型中T细胞成熟相关蛋白（MAL）、细胞黏附分子1（CADM-1）、白细胞介素-6（IL-6）、白细胞介素-8（IL-8）、白细胞介素-33（IL-33）、胸腺基质淋巴细胞生成素（TSLP）、信号传导与转录激活因子（STAT3）的表达。方法：将Balb/c小鼠18只随机分为对照组（A组）、哮喘组（B组）、肝郁型哮喘组（C组），每组各6只。按照慢性不可预知性温和刺激（CUMS）联合氢氧化铝及卵清蛋白（OVA）混合液腹腔注射致敏，OVA雾化激发的方式建立肝郁型哮喘小鼠模型与哮喘小鼠模型。观察造模前后各组小鼠体质量及糖水消耗量、强迫游泳不动时间等指标，以及肺组织病理改变情况。检测肺组织中MAL、CADM-1、IL-6、IL-8、IL-33、TSLP、STAT3蛋白及mRNA的表达。结果：A、C组体质量造模后第7、14、21、28天同时间节点组间比较，差异均有统计学意义（P<0.05）。C组糖水消耗量造模前后比较，差异有统计学意义（P<0.05）。A、C组小鼠强迫游泳不动时间造模后组间比较，差异均有统计学意义（P<0.05）。肺组织病理学结果显示，A组无炎症细胞浸润，B、C组有炎症细胞浸润。B、C组MAL、CADM-1、IL-6、IL-8、IL-33、TSLP的蛋白表达与A组比较，C组IL-6、IL-33的蛋白表达与B组比较，差异均有统计学意义（P<0.05或P<0.01）。B、C组MAL、CADM-1、IL-6、IL-8、IL-33、TSLP的mRNA蛋白表达与A组比较，C组MAL、CADM1、IL-6、IL-8、TSLP的mRNA蛋白表达与B组比较，差异均有统计学意义（P<0.05或P<0.01）。结论：本研究建立的肝郁型哮喘小鼠模型符合中医证候特点和哮喘病理特点，是较理想的肝郁型哮喘模型。肝郁型哮喘小鼠模型中MAL、CADM1表达下调，IL-6、IL-8、IL-33、TSLP表达上调。 |
| 关键词: 哮喘 肝郁型 小鼠 模型建立 实验动物 |
| DOI： |
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| Experimental study of expression of MAL,CADM1,IL-6,IL-8,IL-33,TSLP,and STAT3 in a mouse model of asthma with stagnation of liver Qi |
| ZHENG Xinying,LIU Wei,WU Xiaoling |
| (Hunan University of Chinese Medicine，Changsha 410208，Hunan，China;The Second Affiliated Hospital of University of South China，Hengyang 421001，Hunan，China) |
| Abstract: |
| Objective：To investigate the expression of T-lymphocyte maturation-associated protein (MAL)，cell adhesion molecule 1 (CADM1)，interleukin-6 (IL-6)，interleukin-8 (IL-8)，interleukin-33 (IL-33)，thymic stromal lymphopoietin (TSLP)，and signal transducer and activator of transcription 3 (STAT3) in a mouse model of asthma with stagnation of liver Qi.Methods：A total of 18 Balb/c mice were randomly divided into control group (group A)，asthma group (group B)，and asthma with stagnation of liver Qi group (group C)，with 6 mice in each group.A mouse model of asthma with stagnation of liver Qi and a mouse model of asthma were established by sensitization with chronic unpredictable mild stimulation combined with intraperitoneal injection of the mixed solution of aluminum hydroxide and ovalbumin (OVA) and aerosol challenge with OVA.Related indices were measured before and after modeling，including body weight，sugar water consumption，immobility time in forced swimming test，and lung histopathological changes.The protein and mRNA expression levels of MAL，CADM1，IL-6，IL-8，IL-33，TSLP，and STAT3 in lung tissue were also measured.Results：There was a significant difference in body weight between group A and group C on days 7，14，21，and 28 after modeling (P<0.05).Group C had a significant change in sugar water consumption after modeling (P<0.05).There was a significant difference in immobility time in forced swimming test between group A and group C after modeling (P<0.05).Lung histopathological results showed the absence of inflammatory cell infiltration in group A and the presence of inflammatory cell infiltration in groups B and C.There were significant differences in the protein expression levels of MAL，CADM1，IL-6，IL-8，IL-33，and TSLP between groups B/C and group A，and there were significant differences in the protein expression levels of IL-6 and IL-33 between group C and group B (P<0.05 or P<0.01).There were significant differences in the mRNA expression levels of MAL，CADM1，IL-6，IL-8，IL-33，and TSLP between groups B/C and group A，and there were significant differences in the mRNA expression levels of MAL，CADM1，IL-6，IL-8，and TSLP between group C and group B (P<0.05 or P<0.01).Conclusion：The mouse model of asthma with stagnation of liver Qi established in this study has TCM syndrome characteristics and the pathological features of asthma and is thus a satisfactory model of asthma with stagnation of liver Qi.Downregulation of MAL and CADM1 and upregulation of IL-6，IL-8，IL-33，and TSLP are observed in the mouse model of asthma with stagnation of liver Qi. |
| Key words: asthma stagnation of liver Qi mouse modeling experimental animal |
