CKLF1高表达激活NF-κB信号通路导致小鼠肺部炎症

High expression of CKLF1-induced lung inflammation by NF-κB signal pathway in mice

目的有报道表明趋化素样因子1(CKLF1)在哮喘病人肺部高表达,但具体情况和机制尚不明确。本研究拟在动物水平考察CKLF1的致炎作用及相关机制。方法将pCDB-CKLF1质粒或空载体pCDB电转入Balb/C小鼠体内,HE染色观察其肺部病理改变;硝酸酶还原法和ELISA法分别检测小鼠血清中NO和TNF-α的含量;提取小鼠肺部组织的胞质和胞核蛋白,蛋白免疫印迹实验考察胞质和胞核内NF-κB和IκBα表达的改变。结果病理切片结果显示,转染pCDB-CKLF1质粒后,小鼠肺部出现明显的病理改变;小鼠血清中NO和TNF-α含量明显升高;胞质内NF-κB和IκBα表达明显减少,胞核内NF-κB和IκBα表达明显增加。结论趋化因子CKLF1高表达能够导致动物肺部炎症的发生,CKLF1可能通过激活NF-κB信号通路导致炎症。

Aim To explore the inflammatory mecha- nism of chemokine-like factor 1 （CKLF1） in mice. Methods Mice were transfected with pCDB vector （control group） or pCDB-CKLF1 plasmid （ model group）. Then HE staining, nitrate reductase method and ELISA were adopted to test the pathological chan- ges, the concentration of NO and TNF-α in the serum of mich. The expression of NF-κB and IκBα in lung cytoplasm and nucleus was detected by Western blot. Results Transfection with pCDB-CKLF1 plasmid led to significant lung inflammation in mice, and obviously increased the level of NO and TNF-α in serum cornpared with transfection with pCDB vector in mice. Western blot experiments showed that transfection with pCDB-CKLF1 plasmid could decrease the expression of NF-κB and IκBα in cytoplasm, and increase the expression of NF-κB and IκBα in nucleus compared with transfection with pCDB vector in mice. Conclusions CKLF1 can lead significant lung inflammation in mice. The effect may be related to the activation of NF-κB signaling pathway.