哮喘小鼠肺组织STAT5、STAT6表达及阿奇霉素的影响

目的观察阿奇霉素(AZM)对哮喘小鼠信号转导和转录激活因子5、6(STAT5、STAT6)的影响。方法 BALB/c小鼠24只随机分为三组,A组(哮喘模型组)、B组(阿奇霉素治疗组)、C组(正常对照组)。其中A、B组小鼠于第0、13天分别给予卵清蛋白(OVA)20μg和氢氧化铝1 mg的混悬液致敏,于第21-30天每天给予雾化吸入2%OVA建立哮喘模型,B组于15-30天给予阿奇霉素100 mg/kg/d腹腔注射,C组以0.9%生理盐水代替OVA致敏和激发。所有动物于31天处死,制备肺组织石蜡切片,应用免疫组化方法检测支气管肺组织STAT5、STAT6的表达水平。结果哮喘模型组STAT5、STAT6蛋白表达分别为(23.25±3.28)和(26.11±3.95)明显高于正常对照组(2.33±0.78)和(2.78±0.32)(P0.01),阿奇霉素治疗组STAT5、STAT6蛋白表达分别为(10.83±1.96)和(11.32±2.03)明显低于哮喘组(P0.01)。结论 STAT5S、TAT6与哮喘发病相关,阿奇霉素可通过下调STAT5、STAT6的表达抑制气道炎症。

Effects of Azithromycin on signal transducers and activators5,6 in Asthmatic mice

Objective To observe the effects of azithromycin（AZM） on the expression of STAT5、STAT6 in asthmatic mice models.Methods 24 BALB/c mice were randomly divided into three groups：group A（asthmatic model group）;group B（AZM treated group）;group C（control group）.Mice in group A、B were respectedly sensitized on days 0,13 by Ovalbumin（OVA） 20 μg together with Al（OH）3 1mg and challenged from 21-30 by inhalation of 2%OVA to establish a murine model of asthma.On days 15 to 30,the animals in group B were intraperitoneal injected with AZM（100 mg/kg per day）,Group C was sensitized and challenged by 0.9%NaCl.All the animals were killed on day 31.The paraffin sections of pulmonary tissues were made.The expression of STAT6,STAT5 in lung was analyzed by immunohistochemistry.Results STAT5、STAT6 protein expression in asthmatic model group（23.25±3.28）and（26.11±3.95）significantly increased comparing with the control group（2.33±0.78）and（2.78±0.32）（P0.01） STAT5、STAT6 protein expression in AZM treated group（10.83±1.96）and（11.32±2.03）were significantly lower than asthmatic model group.（P0.01）Conclusion STAT5 and STAT6 are related to the pathogenesis of asthma.The mechanism of AZM suppressing the inflammation of airway in asthmatic model may be explained by that AZM could down regulate the expression of STAT6、STAT5.