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寻常型银屑病皮损中白细胞介素-36细胞因子表达及其与p38丝裂原活化蛋白激酶和核因子κB信号通路的关系

IL-36 cytokine expression and its relationship with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions.

作者信息

He Qi, Chen Hong-Xiang, Li Wen, Wu Yan, Chen Shan-Juan, Yue Qing, Xiao Min, Li Jia-Wen

机构信息

Department of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2013 Aug;33(4):594-599. doi: 10.1007/s11596-013-1164-1. Epub 2013 Aug 1.

Abstract

This study examined the correlation of the expression of interleukin-36 (IL-36), a novel member of interleukin-1 (IL-1) family, with p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36α, IL-36β, IL-36Γ, phosphorylated p38 MAPK, and NF-κBp65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. The cytokine expression levels were compared between the psoriasis group and the control group. A correlation analysis between cytokine proteins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-36β, IL-36Γ, phosphorylated p38 MAPK and NF-κBp65 in the psoriasis group were significantly higher than those in the control group (P<0.001). In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-κBp65 expression (P<0.05). A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-κBp65 expression (P<0.01). It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.

摘要

本研究检测了白细胞介素-1(IL-1)家族新成员白细胞介素-36(IL-36)的表达与寻常型银屑病皮损中p38丝裂原活化蛋白激酶(p38 MAPK)和核因子-κB(NF-κB)信号通路的相关性。采用实时定量逆转录聚合酶链反应(qRT-PCR)和蛋白质免疫印迹法检测38例银屑病患者及17例健康对照者皮肤组织中IL-36α、IL-36β、IL-36γ、磷酸化p38 MAPK及NF-κBp65的表达水平。比较银屑病组和对照组细胞因子表达水平,并对银屑病组细胞因子蛋白进行相关性分析。结果显示,银屑病组IL-36α、IL-36β、IL-36γ、磷酸化p38 MAPK及NF-κBp65的表达水平显著高于对照组(P<0.001)。在银屑病组中,IL-36细胞因子表达与磷酸化p38 MAPK及NF-κBp65表达呈正相关(P<0.05)。磷酸化p38 MAPK与NF-κBp65表达之间也存在显著正相关(P<0.01)。结论:寻常型银屑病皮损中IL-36表达增加与p38 MAPK和NF-κB信号通路相关。这三个因素可能共同参与银屑病的发病机制及局部炎症反应。

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