中华皮肤科杂志

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中波紫外线激活HaCaT细胞炎症信号通路的实验研究

蒋献1, 王国兴2, 吴琦2, 李利1, 冉玉平1   

  1. 1. 四川大学华西医院皮肤科, 成都 610041;
    2. 四川大学基础医学与法医学院感染免疫室
  • 收稿日期:2006-01-05 出版日期:2006-04-15 发布日期:2006-04-15
  • 通讯作者: 冉玉平, email:ranyupin@holmail.com E-mail:ranyupin@holmail.com

Activation of intracellular inflammation signal transduction pathway of HaCaT cells by ultraviolet B

JIANG Xian1, WANG Guo-xing2, WU Qi2, LI Li1, RAN Yu-ping1   

  1. Department of Dermatology, West China Hospital, Sichuan University, Chengdu 610041, China
  • Received:2006-01-05 Online:2006-04-15 Published:2006-04-15

摘要: 目的 探讨中波紫外线(UVB)对角质形成细胞(KC)炎症信号通路的影响.方法 UVB(40 mJ/cm2)照射永生化人角质形成细胞株HaCaT细胞,分别于照射后0、10、30、60、120、240min收集细胞蛋白和核蛋白,蛋白质印迹法检测NF-κB信号传导通路中的重要分子-磷酸化IκB-α(P-IκB-α)、IκB-α和NF-κB p65蛋白的动态变化,以及MAPK家族的蛋白分子ERK1/2、p38、c-JNK等磷酸化激活的动态变化.结果 蛋白质印迹法检测结果显示,UVB照射后0.5h IκB-α开始发生磷酸化和降解,在第2、4小时时更加明显;细胞核蛋白p65的量在照射后0.5h开始升高,在随后的2h时达到高峰.UVB照射后10 min HaCaT细胞内的ERK1/2、p38、c-JNK蛋白的磷酸化就开始增加.结论 UVB照射KC可激活细胞内的NF-κB及MAPK信号传导通路.

关键词: 紫外线, 角蛋白细胞, 信号传导

Abstract: Objective To explore the effects of ultraviolet B (UVB) on signal transduction pathway of HaCaT cells.Methods HaCaT cells,an immortalized human keratinocyte cell line,were irradiated with 40 mJ/cm2 UVB,the cellular and nuclear protein of HaCaT cells was isolated and collected at 0,10,30,60,120,240 min after the irradiation.Western blot was performed to detect the dynamic changes of phosphorylated-IkB-α,IκB-αand NF-κB p65 protein in the nuclei,and the phosphorylation status of MAPK proteins including ERK1/2,p38,c-JNK.Results As shown by the Western blott,the phosphorylation and degradation of IkB-αbegan at 0.5 h,and became more noticeable at 2 h and 4 h,after the UVB irradiation.The level of p65 protein began to increase at 0.5 h,and peaked at 2h after the irradiation.The phosphorylation of ERK1/2,p38,c-JNK increased dramatically as early as 10 min after the UVB irradiation.Conclusion UVB can activate the intracellular signal transduction pathway of MAPK and NF-κB in keratinocytes.

Key words: Ultraviolet rays, Keratinocytes, Signal transduction