丙酮酸乙酯对TDI诱导的哮喘小鼠气道上皮细胞黏附连接蛋白E-cadherin的影响  

Effect of ethyl pyruvate on E-cadherin of airway epithelium in a TDI-induced mouse asthma

作　　者：梁俊杰[1] 唐海雄[1] 赵海金[1] 宋甲富[1] 姚利红[1] 董航明[1] 蔡绍曦[1] 

机构地区：[1]南方医科大学南方医院呼吸与危重症医学科,慢性气道疾病实验室,广州市510515

出　　处：《实用医学杂志》2014年第22期3555-3558,共4页The Journal of Practical Medicine

基　　金：国家自然科学基金(编号:81270087;81270089);国家重点基础研究发展计划("973计划")(编号:2012CB518200);广东省教育部产学研结合项目(编号:2012B091100153);广东省科技计划项目(编号:2011B031800245)

摘　　要：目的:观察丙酮酸乙酯(EP)对甲苯二异氰酸酯(TDI)诱导的哮喘小鼠气道上皮细胞黏附连接蛋白E-cadherin表达的影响。方法:BALB/c小鼠30只,随机分为3组。哮喘组第1天、第8天予0.3%TDI耳背致敏,第15、18、21天予3%TDI激发,每次激发前1 h按100 mg/kg腹腔注射生理盐水。对照组第1天、第8天予AOO(丙酮和橄榄油)致敏,余同哮喘组。EP治疗组,同哮喘组,但在激发前1 h按100 mg/kg腹腔注射EP。第22天检测各组小鼠的气道高反应性、淋巴上清IL-4、IFN-γ及血清Ig E,用免疫组化及WB测定肺组织E-cadherin。结果:哮喘组气道高反应性、淋巴上清IL-4、IFN-γ及血清Ig E均高于对照组,EP干预后显著降低。免疫组化及免疫印迹结果示,对照组E-cadherin均匀致密分布于气道上皮细胞连接处,哮喘组Ecadherin分布混乱、减少,EP干预能显著减少E-cadherin的破坏。结论:EP可以减少TDI诱导的哮喘小鼠气道上皮细胞E-cadherin的破坏。Objective To explore the role of ethyl pyruvate （EP） on E-cadherin of airway epithelium and airway inflammation in a TDI-induced mouse asthma model. Methods 30 male BALB/c mice were randomly divided into control group, asthma group and EP group. On day 1 and 8, mice in asthma group and EP group were treated with 0.3% TDI on the dorsum of both ears for sensitization. And on day 15, 18 and 21 the mice underwent an aerosol inhalation of 3% TDI, and saline （100 mg/kg） was injected intraperitoneally 1 hour before inhalation. The control group underwent acetone and olive oil （AOO） sensitization on day 1 and 8, AOO challenge on day 15, 18 and 21. Saline （100 mg/kg） was injected intraperitoneally 1 hour before challenge. One hour before each challenge, mice were given EP （100mg/kg） or vehicle via intraperitoneal injection. On day 22, airway reactivity, IL-4, IFN-γ and IgE in the serum were detected, immunohistochemistry and WB were used to assess E-cadherin levels. Results Airway reactivity, IL-4, IFN-γ in and IgE in the serum in asthma group are significantly higher than that in control group （P 〈 0.05 ）. Treatment with EP dramatically decreased airway byperresponsiveness in TDI- challenged mice, as well as IL-4, IFN-~/and IgE （P 〈 0.05）. E-cadherin in control group was distributed evenly at the connection of epithelial cells. E-cadherinin distribution was chaotic and its expression was decreased in asthma group. EP intervention can ameliorate the damage of E-cadherinin. Conclusions EP can ameliorate the destruction of E-cadherin in airway epithilum by TDI.

关 键 词：丙酮酸乙酯 TDI哮喘 E-CADHERIN 

分 类 号：R562.25[医药卫生—呼吸系统]