摘要
目的探讨褪黑素(MT)对哮喘小鼠肺组织信号传导子和转录激活子4(STAT4)表达的影响及其在气道炎症中的作用。方法最后1次雾化激发后1 h行左肺支气管肺泡灌洗计数炎性细胞;免疫组织化学和实时定量PCR分别检测右肺组织STAT4蛋白及其mRNA的表达;酶联免疫吸附试验检测外周血IL-12水平。结果 (1)模型组小鼠支气管肺泡灌洗液(BALF)中炎性细胞总数和EOS较对照组明显增多,肺组织STAT4蛋白及其mRNA表达较对照组明显降低;MT组以上指标均得到明显缓解(P<0.01);(2)哮喘小鼠STAT4蛋白及其mRNA的表达均与BALF中EOS呈高度负相关(r=-0.754,r=-0.755;P<0.01),外周血IL-12水平与STAT4蛋白表达呈高度正相关(r=0.742,P<0.01)。结论 MT能通过诱导哮喘小鼠肺组织STAT4基因的转录、翻译,促进外周血IL-12产生,抑制EOS等炎性细胞浸润,显著抑制气道炎症。
Objective To investigate the effect of melatonin （MT） on signal transduction and activation on transcription 4 （STAT4） and impact on airway inflammation of asthmatic mice. Methods One hour after the last aerosol exposure, the left lungs were lavaged, the number of inflammatory cells in the mouse bronchoaleolar lavage fluids （BALF） were counted with microscope. Using immunohistochemistry and real-time fluorescent quantitative PCR to detect the expression of STAT4 protein and its mRNA expressionism in right lung tissue. Using enzyme-linked immunosorbent assay to detecte levels of IL-12 in serum. Results （ 1 ） In test group, the number of inflammatory cells and EOS were significantly higher than control group, STAT4 protein and STAT4 mRNA expression in lung tissue was significantly decreased when compared with control group. MT treated group significantly alleviated the abovementioned parameters. And there were significant differences between MT treated group and control group, DXM treated group and model group. （P 〈0. 01 ）. （2）In asthmatic mice, STAT4 protein and its mRNA expression had both altitude negative relationship with EOS counts in BALF （ r = 0. 754, P 〈 0. 01 ; r = 0. 755, P 〈 0. 01, respectively）. Levels of IL-12 in serum had altitude positive correlation with STAT4 protein expression in asthmatic group mice （ r = 0. 742, P 〈 0. 01 ）. Conclusion MT may induce STAT4 gene transcription and translation in asthmatic mice, so promotes production of IL-12 in peripheral blood and inhibits inflammatory cell infiltration.
出处
《基础医学与临床》
CSCD
北大核心
2011年第2期179-182,共4页
Basic and Clinical Medicine
基金
宜昌市2010年医疗卫生科技计划(A01301-09)
