肿瘤坏死因子-α诱导蛋白8样分子-2通过NF-κB信号通路影响LPS诱导的支气管上皮细胞分泌炎症因子

Tumor necrosis factor-αinduced protein 8 like 2 affects LPS induced secretion of inflammatory factors by NF-κB signaling pathway

目的:探讨肿瘤坏死因子-α诱导蛋白8样分子-2(TIPE2)对脂多糖(LPS)诱导的支气管上皮细胞分泌炎症因子的影响和机制。方法:以人支气管上皮细胞作为探讨对象,用RT-PCR和Western blot方法检测LPS处理对支气管上皮细胞中TIPE2表达影响。在人支气管上皮细胞中转染TIPE2过表达载体,给予LPS处理,ELISA方法检测细胞分泌IL-6、IL-8、IL-1β含量变化;Western blot方法测定细胞中NF-κBp65、p-ⅠκBαSer 32蛋白表达变化。以NF-κB激活剂处理过表达TIPE2的支气管上皮细胞,用上述方法测定细胞分泌IL-6、IL-8、IL-1β和NF-κBp65、p-ⅠκBαSer 32蛋白表达变化。结果:LPS处理后的支气管上皮细胞中TIPE2表达水平显著下降。LPS处理后支气管上皮细胞分泌的IL-6、IL-8、IL-1β含量增多,细胞中NF-κBp65、p-IκBαSer 32蛋白表达增多。过表达TIPE2可以显著抑制LPS诱导的支气管上皮细胞分泌IL-6、IL-8、IL-1β、NF-κBp65和p-ⅠκBαSer 32蛋白表达。NF-κB激活剂处理可以逆转过表达TIPE2对LPS条件下支气管上皮细胞分泌IL-6、IL-8、IL-1β、NF-κBp65和p-ⅠκBαSer 32蛋白表达的影响。结论:TIPE2通过抑制NF-κB信号激活阻碍LPS诱导的支气管上皮细胞分泌炎症因子。

Objective:To investigate the effect and mechanism of tumor necrosis factor-αinduced protein 8 like 2(TIPE2)on the secretion of inflammatory factors in bronchial epithelial cells induced by lipopolysaccharide(LPS).Methods:Human bronchial epithelial cells were used as the research object,the effect of LPS treatment on the expression of TIPE2 in bronchial epithelial cells was detected by RT-PCR and Western blot.TIPE2 overexpression vector was transfected into human bronchial epithelial cells,give LPS treatment,the changes of IL-6,IL-8 and IL-1βwere detected by ELISA;the expression of NF-κBp65 and p-ⅠκBαSer 32was measured by Western blot.The bronchial epithelial cells overexpressed with TIPE2 were treated with NF-κB activator,the changes of IL-6,IL-8,IL-1β,NF-κBp65 and P-ⅠκBαSer 32were measured by the above methods.Results:After LPS treatment,the expression level of TIPE2 in bronchial epithelial cells decreased significantly.After LPS treatment,the contents of IL-6,IL-8,IL-1βand the expression of NF-κBp65,P-ⅠκBαSer 32protein increased.Overexpression of TIPE2 significantly inhibited LPS induced secretion of IL-6,IL-8,IL-1βand expression of NF-κBp65,p-ⅠκBαSer 32.NF-κB activator treatment could reverse the effect of overexpression of TIPE2 on the secretion of IL-6,IL-8,IL-1βand the expression of NF-κBp65,p-ⅠκBαSer 32in LPS treated bronchial epithelial cells.Conclusion:TIPE2 inhibits secretion of inflammatory factors induced by LPS through inhibiting NF-κB signal activation.