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目的研究白细胞介素-13(IL-13)在体内对支气管/肺黏液分泌的作用并探讨其作用机制。方法所有SD大鼠被随机分为IL-13组、对照组和IL-13 plus SP600125组。Western检测大鼠支气管/肺组织黏蛋白(MUC)5AC,磷酸化细胞外信号调节激酶1/2(p-ERK1/2)和磷酸化c-Jun氨基端激酶1/2(p-JNK1/2)的表达变化,RT-PCR检测大鼠支气管/肺组织STAT4和STAT6 mRNA表达水平。EMSA检测通路下游作用因子FOXA2和激活蛋白1的表达。结果同对照组相比,IL-13刺激10 h后大鼠支气管/肺组织MUC5AC和p-JNK1/2表达升高,而p-ERK1/2表达无显著变化;使用SP600125阻断JNK通路表达后,MUC5AC表达减弱;IL-13刺激10 h后大鼠支气管/肺组织STAT4 mRNA表达无显著变化,STAT6 mRNA表达显著升高,EMSA提示IL-13刺激后大鼠支气管/肺组织FOXA2结合活性显著降低,而激活蛋白1结合活性没有明显变化。结论 IL-13能够刺激大鼠支气管/肺组织黏液分泌,其作用机制可能是通过调控STAT6-FOXA2信号通路。
Objective To study the effect of interleukin-13 (IL-13) on bronchial / pulmonary mucus secretion in vivo and to explore its mechanism. Methods All SD rats were randomly divided into IL-13 group, control group and IL-13 plus SP600125 group. Western blot was used to detect the expression of 5AC, p-ERK1 / 2 and p-JNK1 / 2 ), And the expression of STAT4 and STAT6 mRNA in bronchus / lung tissue of rats were detected by RT-PCR. Downstream EMSA signaling pathway expression of FOXA2 and activator protein 1. Results Compared with the control group, the expressions of MUC5AC and p-JNK1 / 2 in bronchus / lung tissue were increased and the expression of p-ERK1 / 2 was not significantly changed after IL-13 stimulation for 10 h. The expression of JNK pathway was blocked by SP600125 , And the expression of STAT5 mRNA in bronchus / lung tissue of IL-13-stimulated rats was not significantly changed after 10-hour stimulation with IL-13, and EMSA indicated that FOXA2 binding activity in bronchus / lung tissue was significantly decreased after IL-13 stimulation , While Activin-1 binding activity did not change significantly. Conclusion IL-13 can stimulate the mucosal secretion of bronchial / lung tissue in rats, and its mechanism may be through the regulation of STAT6-FOXA2 signaling pathway.