CAJ | 학술논문

目的观察白细胞介素-22 (IL-22)对缺氧肠上皮T84细胞屏障功能的影响,探讨其分子机制.方法对T84细胞进行2％02缺氧6h(Hx组)及100 μg/L重组IL-22(Hx+ rIL-22)处理,分别检测跨上皮电阻(TER),IL-22受体A1(IL-22RA1)及紧密连接蛋白:ZO-1、Occludin、Claudin-1及Claudin-4的mRNA与蛋白表达.结果缺氧引起IL-22RA1的mRNA及蛋白表达较常氧分别下降30.0％及63.0％,并引起TER降低54.7％,经rIL-22预处理使得TER较Hx升高43.8％.缺氧处理使ZO-1、Occludin、Claudin-1及Claudin-4表达明显降低,而rIL-22预处理则可缓解该现象(mRNA及蛋白表达较Hx组分别升高:44.3％、36.4％、77.6％、61.2％及109.3％、77.6％、153.3％、79.6％,P＜0.01).结论 IL-22与其受体作用后可以维持肠屏障功能,稳定渗透性,调控紧密连接蛋白的表达.
목적 관찰백세포개소-22 (IL-22)대결양장상피T84세포병장공능적영향,탐토기분자궤제.방법 대T84세포진행2％02결양6h(Hx조)급100 μg/L중조IL-22(Hx+ rIL-22)처리,분별검측과상피전조(TER),IL-22수체A1(IL-22RA1)급긴밀련접단백:ZO-1、Occludin、Claudin-1급Claudin-4적mRNA여단백표체.결과 결양인기IL-22RA1적mRNA급단백표체교상양분별하강30.0％급63.0％,병인기TER강저54.7％,경rIL-22예처리사득TER교Hx승고43.8％.결양처리사ZO-1、Occludin、Claudin-1급Claudin-4표체명현강저,이rIL-22예처리칙가완해해현상(mRNA급단백표체교Hx조분별승고:44.3％、36.4％、77.6％、61.2％급109.3％、77.6％、153.3％、79.6％,P＜0.01).결론 IL-22여기수체작용후가이유지장병장공능,은정삼투성,조공긴밀련접단백적표체.
Objective To investigate the effect of interleukin-22 (IL-22) on intestinal barrier function of T84 cells under hypoxia and the molecular mechanism.Methods T84 cells were randomly divided into 3 groups:the normoxia group (Nx),the hypoxia group (Hx,2％ O2 for6 h) and hypoxia plus 100 μg/L rIL-22 group (Hx + rIL-22).Transepithelial electrical resistance (TER) was determined,and the protein and mRNA expression of IL-22 receptor A1 (IL-22RA1) was detected.zonula occludens-1 (ZO-1),Occludin,Claudin-1 and Claudin-4 expression was examined by using reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.Results Both mRNA and protein expression levels of IL-22RA1 were significantly reduced by 30.0％ and 63.0％ respectively in Hx group as compared with Nx group (P ＜ 0.01).The TER value in Hx group was decreased by 54.7％ as compared with Nx group (P ＜ 0.01),which could be reversed through the pretreatment of rIL-22 (P ＜ 0.01).The expression levels of ZO-1,Occludin,Claudin-1 and Claudin-4 in Hx group were lower than in Nx group (P ＜0.01),but pretreatment with rIL-22 could attenulate the decreased expression of TJs under hypoxia (P ＜0.01).Conclusion After binding to its receptor complex,IL-22 could maintain the epithelial barrier function through regulating the expressionof TJs.