摘要
目的:探讨晚期糖化终产物(AGEs)与晚期糖化终产物受体(RAGE)结合对Jurkat细胞分泌肿瘤坏死因子-α(TNF-α)的影响及相关信号分子的变化。方法:不同浓度AGEs作用于植物血球凝集素(PHA)预刺激的Jurkat细胞24小时,MTT检测AGEs对细胞生存率的影响,ELISA检测AGEs诱导Jurkat细胞分泌TNF-α;Western blot检测AGEs诱导Jurkat细胞表达RAGE和p38MAPK、JNK磷酸化水平。结果:AGEs作用于PHA预刺激Jurkat细胞24小时对细胞生存率无明显影响;AGEs促进Jurkat细胞表达RAGE,增加炎症因子TNF-α分泌,抗RAGE抗体明显抑制AGEs诱导的TNF-α分泌。AGEs可引起p38MAPK、JNK磷酸化,p38MAPK、JNK的抑制剂明显抑制AGEs诱导的TNF-α表达。结论:AGEs通过RAGE促进PHA预刺激的Jurkat细胞分泌炎症因子TNF-α,其机制与激活p38MAPK、JNK途径有关。
Objective：To investigate the role of AGEs-RAGE on the expression of TNF-a and associated signaling pathway in Jurkat cells. Methods：MTT was used to detect viability of Jurkat cells cubated by AGEs. The expression of RAGE was assessed by Western blot and the secretion of TNF-a was tested by ELISA. In addition, total and phosphorylated p38MAPK, JNK were measured using Western blot when Jurkat cells were treated AGEs. Results：No changes in cell viability were observed when Jurkat cells were treated AGEs or BSA for 24 h. AGEs enhanced the expression of RAGE in Jurkat cells. AGEs induced the expression of TNF-a which was inhibited by pre-treatment with anti-RAGE. In addition, incubation of Jurkat cells with AGEs results in significant increase in p38MAPK, JNK phosphorylation. Treatment with p38MAPK inhibitor or JNK inhibitor inhibited AGEs-induced TNF-a expression. Conclusion：AGEs promote TNF-a expression in Jurkat cells via RAGE, p38 MAPK and JNK signal pathway.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2012年第7期594-598,共5页
Chinese Journal of Immunology
基金
福建省医学创新课题资助项目(2011-CXB-7)
关键词
晚期糖化终产物受体
JURKAT细胞
炎症因子
信号转导
Receptor, advanced glycation endproduct
Jurkat cells
Inflammatory eytokine
Signal transduction
