
FOLLOWUS
1. 1 Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China
2. 2 Department of Dermatology, Dermatology Hospital of Southern Medical University, Guangdong Provincial Dermatology Hospital, Guangdong 510080, China
*Tel & Fax: 86-10-69151502, E-mail: jinhongzhong@263.net
收稿日期:2018-12-28,
网络出版日期:2019-09-30,
纸质出版日期:2019-09-30
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王文明, 吴超, 余晓玲, 等. 白细胞介素-36
Wang Wenming, Wu Chao, Yu Xiaoling, et al. IL-36
王文明, 吴超, 余晓玲, 等. 白细胞介素-36
Wang Wenming, Wu Chao, Yu Xiaoling, et al. IL-36
目的
银屑病是一种免疫介导的炎症性疾病。尽管目前银屑病的研究取得了巨大的进展
但其确切机制尚不完全清楚。表皮的增殖异常在银屑病的发病中发挥重要作用。本研究将在体外探究白细胞介素-36β(IL-36β)对角质形成细胞功能的影响。
方法
体外培养人永生化角质形成细胞系HaCaT
分为3组:对照组、50 ng/ml IL-36
β
组、100 ng/ml IL-36
β
组
分别处理24 h。采用CCK8法检测细胞增殖
流式细胞术检测细胞凋亡与细胞周期分布
实时荧光定量PCR检测角质形成细胞分化指标keratin 10 mRNA和involucrin mRNA的表达
ELISA法检测培养液中炎症因子IL-1β和IL-6的含量。
结果
与对照组相比
50、100 ng/ml IL-36
β
可使HaCaT细胞阻滞在S期(
P
<
0.05);同时可抑制细胞keratin 10、involucrin mRNA的表达(
P
<
0.01);100 ng/ml IL-36
β
可增加细胞培养液中IL-1
β
与IL-6的含量(
P
<
0.05)。
结论
IL-36
β
可能导致角质形成细胞周期阻滞
抑制角质形成细胞分化
促进角质形成细胞的炎症反应。
Objective
Psoriasis is an immune-mediated inflammatory disease. Despite advances in the study of its pathogenesis
the exact development mechanism of psoriasis remains to be fully elucidated. Hyperproliferative epidermis plays a crucial role in psoriasis. This study aimed to investigate the effects of interleukin-36
β
(IL-36
β
) on keratinocyte dysfunction
in vitro
.
Methods
Human keratinocyte cell lines
HaCaT cells
were treated with 0 (control)
50 or 100 ng/ml IL-36
β
respectively for 24 h. Cell viability was determined with a cell counting kit-8 assay. Flow cytometry was used to assess the effects of IL-36
β
on apoptosis and cell cycle distribution. Expressions of the differentiation markers
such as keratin 10 and involucrin
were evaluated by quantitative real-time polymerase chain reaction (RT-qPCR). Expressions of the inflammatory cytokines
IL-1
β
and IL-6 were tested by ELISA.
Results
CCK8 assay showed the survival rate had no significant difference between the control and treated group (
P
>
0.05). Flow cytometry analysis showed cell cycle arrest at S phase in the IL-36
β
-treated groups compared with the control group (
P
<
0.05). RT-qPCR verified the decreased mRNA expressions of keratin 10 and involucrin in the IL-36
β
-treated groups compared with the negative control (
P
<
0.01). ELISA showed 100 ng/ml IL-36
β
enhanced levels of IL-1
β
and IL-6 in culture supernatants of HaCaT cells compared with the negative control (
P
<
0.05).
Conclusion
Taken together
these findings suggest that IL-36
β
could induce cell cycle arrest at S phase
inhibit keratin 10 and involucrin expressions and promote inflammatory activity in HaCaT cell lines.
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