中国麻风皮肤病杂志 ›› 2020, Vol. 36 ›› Issue (9): 519-522.doi: 10.12144/zgmfskin202009519

• 论著 • 上一篇    下一篇

卡泊三醇对TNF-α诱导的人角质形成细胞中CCL20表达的影响

王岚琦1,杨梦波1,王孝盼2,鞠强1   

  1. 1上海交通大学医学院附属仁济医院皮肤科，上海，200127；2上海交通大学医学院附属瑞金医院皮肤科，上海，200025
  • 出版日期:2020-09-15 发布日期:2020-08-21
  • 通讯作者: 鞠强，E-mail: qiangju@aliyun.com

Effect of calcipotriol on CCL20 expression induced by TNF-α in human keratinocytes

WANG Lanqi1, YANG Mengbo1, WANG Xiaopan2, JU Qiang1   

  1. 1 Department of Dermatology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, China; 2 Department of Dermatology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China
  • Online:2020-09-15 Published:2020-08-21
  • Contact: JU Qiang, E-mail: qiangju@aliyun.com

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摘要： 目的：明确卡泊三醇体外对TNF-α诱导的人角质形成细胞CCL20表达的影响。方法：体外培养人角质形成细胞，分为TNF-α 组，卡泊三醇组，TNF-α+卡泊三醇组，TNF-α+卡泊三醇+SB202190(p38 MAPK抑制剂)组，TNF-α+卡泊三醇+SP600125(JNK抑制剂)组，TNF-α+卡泊三醇+U0126(ERK抑制剂)组，TNF-α+卡泊三醇+CAPE(NF-κB抑制剂)组。实时荧光定量PCR法和酶联免疫吸附试验检测CCL20 mRNA及蛋白表达水平。Western blot法检测p38 MAPK，ERK和NF-κBp65磷酸化情况。结果：TNF-α+卡泊三醇组CCL20的表达水平及ERK，p38 MAPK，NF-κBp65磷酸化水平低于TNF-α组，差异均有统计学意义（均P<0.05）。TNF-α+卡泊三醇组CCL20的表达水平低于TNF-α+卡泊三醇+U0126(ERK抑制剂)组，高于TNF-α+卡泊三醇+SB202190(p38 MAPK抑制剂)组和TNF-α+卡泊三醇+CAPE(NF-κB抑制剂)组，差异均有统计学意义（均P<0.05）。CCL20的表达水平在TNF-α+卡泊三醇组与TNF-α+卡泊三醇+SP600125(JNK抑制剂)组间比较差异无统计学意义（P>0.05）。结论：卡泊三醇可能通过调节TNF-α诱导的ERK，p38 MAPK，NF-κBp65磷酸化，从而参与调节人角质形成细胞中CCL20表达。

关键词: 卡泊三醇, TNF-α, CCL20, MAPKs, NF-κB

Abstract: Objective: To deremine the effect of calcipotriol on the expression of CCL20 induced by TNF-α in human keratinocytes. Methods: The keratinocytes were cultured in vitro, and then, were divided into TNF-α group, calcipotriol group, TNF-α+calcipotriol group, TNF-α+calcipotriol+SB202190 (p38 MAPK inhibitor) group, TNF-α+calcipotriol+SP600125 (JNK inhibitor) group, TNF-α+calcipotriol+U0126 (ERK inhibitor) group and TNF-α+calcipotriol+CAPE (NF-κB inhibitor) group. The expression level of CCL20 mRNA and protein was detected by real time-QPCR and ELISA. The phosphorylation status of p38 MAPK and ERK and NF-κBp65 was detected by Western blot. Results: The level of CCL20 and phosphorylation levels of p38 MAPK，ERK and NF-κBp65 in TNF-α+calcipotriol group were lower than in TNF-α group, with significant differences (Ps<0.05). The level of CCL20 in TNF-α+calcipotriol group was lower than in TNF-α+calcipotriol+U0126 (ERK inhibitor) group, higher than those in TNF-α+calcipotriol+ SB202190 (p38 MAPK inhibitor) group and CAPE (NF-κB inhibitor) group, with significant differences (Ps<0.05). There was no significant difference in CCL20 level between TNF-α+calcipotriol group and TNF-α+calcipotriol+SP600125 (JNK inhibitor) group. Conclusion: Calcipotriol can inhibit the CCL20 expression induced by TNF-α in keratinocytes, which may be through regulating ERK, p38 MAPK and NF-κB p65 phosphorylation.

Key words: calcipotriol, TNF-α, CCL20, MAPKs, NF-κB