• 关键词：邻苯二甲酸二乙基己酯  卵清蛋白  小鼠  IL-17A  肺功能  气道重塑

• 基金项目：国家自然科学基金重点项目(No.51136002)

• 尤会会
• 华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉 430079

• 赵静云
• 华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉 430079

• 袁烨
• 华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉 430079

• 魏晨曦
• 华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉 430079

• 袁均林
• 华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉 430079

• 摘要：为探讨邻苯二甲酸二乙基己酯(di-(2-ehtylhexyl)phthalate, DEHP)在单独染毒和与卵清蛋白(ovalbumin, OVA)联合染毒条件下对小鼠气道的影响及其相关机制,将Balb/c小鼠随机分为:未处理对照组(生理盐水组)、DEHP染毒组、OVA染毒组、DEHP+OVA联合染毒组(DEHP+OVA),每组雄性Balb/c小鼠6只.用OVA致敏加激发的方式制作小鼠哮喘模型.DEHP染毒组每天给予10 mg·kg^-1 DEHP灌胃,连续54 d.OVA染毒组、DEHP+OVA染毒组小鼠均在第54～60 d(共计1周)进行1% OVA雾化(30 min·d^-1),每日1次,诱发哮喘.第60 d进行以下操作:肺功能测试,肺泡灌洗液(bronchoalveolar lavage fluid, BALF)样品收集和肺组织中的Interleukin-17A(IL-17A)含量的测定.结果显示,与DEHP染毒组相比,DEHP与OVA联合染毒组小鼠BALF的IL-17A显著增加(p<0.05),肺功能降低(p<0.05),气道重塑,肺部细胞浸润明显.提示DEHP对小鼠哮喘模型佐剂作用的分子机制可能涉及IL-17的介导作用.

• Abstract：To explore the effects and the related mechanism of di-(2-ehtylhexyl)phthalate (DEHP) on mice airway with and without ovalbumin (OVA) combined exposure, 24 male balb/c mice were randomly divided into four groups, with each group containing 6 mice: 1Untreated control (saline) group, 2DEHP exposure group, 3OVA exposure group and 4DEHP and OVA combined exposure group. The mouse asthma model was developed by OVA sensitization and challenge.The DEHP exposure group was given 10 mg·kg^-1 DEHP daily by gavage for 54 consecutive days.The OVA exposure group and DEHP+OVA exposure group were given aerosol challenges in 1% OVA (30 min·d^-1) once a day for a week from the 54th day to the 60th day to induce the asthma syndrome. On the 60th day, lung function testing, bronchoalveolar lavage fluid (BALF) collection and lung tissue interleukin-17A (IL-17A) measurement were undertaken. The results demonstrated that compared with DEHP exposure group, the DEHP+OVA exposure group increased IL-17A content significantly (p<0.05), reduced lung function (p<0.05), airway remodeling and pulmonary cells infiltration. It is suggested that the mechanism of DEHP induced asthma may be involved in IL-17 mediated effect.

• Key words：di-(2-ehtylhexyl) phthalate  ovalbumin  mouse, interleukin-17  lung function  airway remodeling

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