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机构地区:[1]泸州医学院附属医院呼吸内科,四川泸州646000
出 处:《泸州医学院学报》2009年第1期9-13,共5页Journal of Luzhou Medical College
摘 要:目的:研究leptin、STAT3及IL-6在哮喘大鼠肺组织的表达,探讨白三烯受体拮抗剂孟鲁司特对leptin,STAT3和IL-6的影响。方法:24只SD大鼠随机分为正常对照组、支气管哮喘组和孟鲁司特组,每组8只,用新鲜配制的混悬液(100mgOVA和100mg氧氧化铝干粉加入1ml生理盐水)制成,第一天腹腔注射致敏,然后第15天起超声雾化吸人1%的OVA.生理盐水激发,每天20分钟,一共7天,建立支气管哮喘动物模型。孟鲁司特组在激发哮喘前1.5小时用孟鲁斯特溶于蒸馏水中灌胃1mg/只。末次激发后,左肺做肺泡关灌洗后取右肺中叶组织做免疫组织化学染色。结果:细胞因子leptin、STAT3和IL-6在支气管上皮呈阳性表达,哮喘组表达比正常组明显增多,leptin在孟鲁司特组表达比哮喘组更加增强,而STAT3和IL-6在孟鲁司特组表达都减少。结论:leptin,STAT3和IL-6可能都参与了哮喘气道免疫炎症过程;孟鲁司特可调控JAK-STAT3途径和IL-6的表达,但不能抑制leptin在气道的表达。Objective:The aim is to study the expression of leptin,STAT3,IL-6 and the relationship between each other in asthma rats and to approach the effectness of leukotrienes-receptor antagonist on leptin-STAT3 pathway,and the relationship with IL-6.Methods: Grouping and Immunization of SD rat: Twenty-four SD rat were divided randomly into normal control group, asthma group and montelukast control group. Experimental SD rat were sensitized with fresh made suspension.(100mg OVA and 100mg aluminum hydroxide adsorbed into lml saline) in the first day,and ultrasonic nebulization with 1% OVA saline was given after 15 days to establish allergen-induced allergic airway inflammation mouse model. Detection of leptin,STAT3 and IL-6 in lung by immunohistochemistry staining.Results:The expression of leptin STAT3 and IL-6 in lung was higher in asthma group than in normol group. Montelukast increased the expression of leptin in lung, but reduced the expression of STAT3 and IL-6 in lung. Conclusion :The expression of leptin,STAT3 and IL-6 were incresed significantly in asthmatic rats compared with normal rats. It can conclude that they are involved in airway inflammation immune process.Montelukast can regulate the jak-STAT3 way and the expression of IL-6,but it can not inhibit the expression of leptin in the airway.
关 键 词:哮喘 瘦素 信号转导和转录激活因子3 白细胞介素6 孟鲁司特
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