中国麻风皮肤病杂志 ›› 2021, Vol. 37 ›› Issue (5): 271-275.doi: 10.12144/zgmfskin202105271

• 论著 • 上一篇    下一篇

IL-17A对角质形成细胞胰岛素抵抗的影响

孙杰,王睿,黄敏,柏佳,李承新   

  1. 中国人民解放军总医院第一医学中心皮肤科，北京，100853
  • 出版日期:2021-05-15 发布日期:2021-04-29
  • 通讯作者: 李承新，E-mail: chengxinderm@163.com

Effect of IL-17A on insulin resistance in keratinocytes

SUN Jie, WANG Rui, HUANG Min, BAI Jia, LI Chengxin   

  1. Department of Dermatology, the First Medical Center, Chinese PLA General Hospital, Beijing 100853, China

  • Online:2021-05-15 Published:2021-04-29
  • Contact: LI Chengxin, E-mail: chengxinderm@163.com

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摘要： 目的：研究IL-17A对角质形成细胞胰岛素抵抗的影响并分析胰岛素抵抗与银屑病病情严重程度的相关性。方法：（1）50 ng/mL的IL-17A刺激HaCaT细胞，Western印迹法检测胰岛素受体下游信号通路蛋白的表达；Western印迹法和细胞免疫荧光法检测GLUT4的表达；（2）对我院2019年1月至2019年12月收治的22例寻常型银屑病患者进行PASI评分，计算患者胰岛素抵抗指数（HOMA-IR）；采用免疫组织化学法检测患者皮损中p-IRS-1（Ser636）的表达，并分析与PASI评分、HOMA-IR的相关性。结果：与胰岛素刺激组比较， 胰岛素刺激+IL-17A组中HaCaT细胞p-IRS-1（Ser636）/IRS-1的表达升高，p-PKB（Ser437）/PKB和GLUT4的表达降低（均P<0.05）；p-IRS-1（Ser636）组织化学评分与患者PASI评分、HOMA-IR均呈正相关（r=0.456，P=0.033；r=0.613，P=0.004）。结论：IL-17A可能通过抑制HaCaT细胞IRS-1/PI3K/PKB/GLUT4信号通路，介导角质形成细胞的胰岛素抵抗，从而可能对银屑病的病情严重程度产生一定影响。

关键词: 银屑病, 白细胞介素17A, 角质形成细胞, 胰岛素抵抗

Abstract: Objective: To evaluate the effect of IL-17A on insulin resistance in keratinocytes and the relationship of keratinocyte insulin resistance with the severity of psoriasis. Methods: HaCaT cells were treated with 50 ng/mL IL-17A, and then Western blot analysis was performed to detect the expression level of downstream proteins of insulin receptors signaling pathways. The expression level of GLUT4 was detected by Western blot and cellular immunofluorescence. The PASI score was assessed and homeostasis model insulin resistance index (HOMA-IR) was calculated in 22 psoriasis patients in our hospital from January to Decemner 2019. The expression of p-IRS-1 (Ser636) in the lesions of patients was detected by immunohistochemistry. And then the correlations between the histochemistry score(H-score) and PASI, HOMA-IR were analyzed. Results: Compared with insulin group, the expression of p-IRS-1 (Ser636)/IRS-1 increased in the insulin+IL-17A group, and the expression of p-PKB (Ser437)/PKB and GLUT4 in HaCaT cells decreased (Ps<0.05). There was a positive correlation between H-score and PASI (r=0.456, P=0.033), and H-score was also positively correlated with HOMA-IR (r=0.613, P=0.004). Conclusion: IL-17A may induce the insulin resistance in HaCaT cells by suppressing the IRS-1/PI3K/PKB/GLUT4 signaling pathway, which may have a certain impact on the severity of psoriasis.

Key words: psoriasis, Interleukin-17A, keratinocyte, insulin resistance