CAJ | 학술논문

近年来邻苯二甲酸酯污染已成为中国一个重要的环境问题.为探讨邻苯二甲酸二乙基己酯(di-(2-ethylhexyl)phthalate,DEHP)在诱发哮喘方面的作用,及研制DEHP诱导大鼠哮喘模型,将32只Wistar大鼠随机分成4组(每组8只):生理盐水对照组、卵清白蛋白(OVA)致敏组和2个DEHP染毒组,采用OVA致敏加激发的方法制作大鼠哮喘模型.2个DEHP染毒组大鼠每天分别进行0.7mg·kg-1和70mg·kg-1邻苯二甲酸二乙基己酯灌胃染毒,连续30d.OVA致敏组、DEHP染毒组大鼠均在第31～37天给予1%OVA雾化,诱发哮喘.第38天取肺脏做组织切片,进行分析.结果表明,与OVA组相比,DEHP染毒组气管壁增厚,细胞浸润增加,气道重塑,特别是在70mg·kg-1·d-1组,变化更为明显.由此可以得出结论,邻苯二甲酸二乙基己酯可诱导哮喘模型大鼠气道重塑,在诱发哮喘发病过程中可能起到佐剂作用.
근년래린분이갑산지오염이성위중국일개중요적배경문제.위탐토린분이갑산이을기기지(di-(2-ethylhexyl)phthalate,DEHP)재유발효천방면적작용,급연제DEHP유도대서효천모형,장32지Wistar대서수궤분성4조(매조8지):생리염수대조조、란청백단백(OVA)치민조화2개DEHP염독조,채용OVA치민가격발적방법제작대서효천모형.2개DEHP염독조대서매천분별진행0.7mg·kg-1화70mg·kg-1린분이갑산이을기기지관위염독,련속30d.OVA치민조、DEHP염독조대서균재제31～37천급여1%OVA무화,유발효천.제38천취폐장주조직절편,진행분석.결과표명,여OVA조상비,DEHP염독조기관벽증후,세포침윤증가,기도중소,특별시재70mg·kg-1·d-1조,변화경위명현.유차가이득출결론,린분이갑산이을기기지가유도효천모형대서기도중소,재유발효천발병과정중가능기도좌제작용.
Phthalate pollution becomes an environmental health problem in China recent years. In order to investigate the potential role of di-(2-ethylhexyl) phthalate (DEHP)in the pathogenesis of asthma and to establish the animal models of DEHP-induced asthma, 32 Wistar rats in four experimental groups were exposed to: (I) saline, (2) ovalbumin (OVA), (3) OVA+DEHP (0.7mg·kg-1·d-1) and (4) OVA+DEHP (70mg·kg-1·d-1). DEHP exposure treatment in this study was undertaken by gastric gavages and done before and during the process of OVA immunization. Lung histological analysis was conducted after. The results showed that, compared with the OVA exposure only, DEHP exposure could increase inflammatory cells infiltration and airway wall thickness significantly; these changes of airway structure in 70r· kg-1·d-1 group were more serious than those in 0.7mg ·kg-1·d-1 group. Therefore, we conclude that DEHP can induce airway remodeling in asthma model and provide an adjuvant role in the pathogenesis of DEI-IP-induced asthma.