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IL-33对人永生化角质形成细胞系和模型小鼠银屑病样皮损的影响 被引量:5

Effects of IL-33 on HaCAT cell line and psoriasis-like lesion in mouse model
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摘要 目的观察白细胞介素-33(IL-33)对人永生化角质形成细胞系(HaCAT)和咪喹莫特(IMQ)诱导的小鼠银屑病样皮损的影响,并对其可能的机制进行探讨。方法不同浓度IL-33刺激HaCAT细胞;CCK8法检测细胞增殖;Western blot检测细胞中LC3、Beclin1和p-STAT3的表达。将BALB/c雌性小鼠随机分为:正常对照组、IMQ组(背部外涂5%咪喹莫特乳膏,建立银屑病样皮损模型)和IL-33处理组(腹腔注射IL-33)。Western blot检测皮损组织中自噬相关蛋白的表达。结果与对照组相比,25 ng/mL的IL-33处理组促进HaCAT细胞的增殖作用最明显(P<0.05),同时,IL-33可促进LC3、Beclin1和p-STAT3蛋白的表达(P<0.05)。在小鼠银屑病样模型中,与正常对照组相比,IMQ组小鼠背部出现鳞屑和红斑伴有表皮增厚,而IL-33处理组与IMQ组相比小鼠背部皮损鳞屑、红斑及增厚更明显(P<0.01)。IL-33处理组皮损中自噬相关蛋白的表达水平低于IMQ组(P<0.05),p-STAT3蛋白的表达水平均高于正常对照组和IMQ组(P<0.05)。结论IL-33促进HaCAT细胞的增殖,诱导细胞自噬,加重咪喹莫特诱导的小鼠银屑病样皮损的发生和发展,其机制可能是通过引起STAT3信号通路的活化而实现的。 Objective To investigate the effects of interleukin-33(IL-33)on HaCAT cells and psoriasis-like inflammation induced by imiquimod(IMQ) in mice. Methods Twenty-four hours after HaCAT cells were plated, the cell proliferation and autophagy-related protein were detect by CCK8 and Western blot. A psoriasis-like lesion model was established in mouse. Thirty female BALB/c mice of clean grade were randomly divided into three groups: control group, IMQ group, and IL-33 treatment group. After 6 days of continuous treatment, the lesions on the back of the mouse were observed. Results The treatment of IL-33 could enhance the proliferation of HaCAT cells and promote the expression of LC3, Beclin1 and p-STAT3 proteins. In the mouse psoriasis-like model, the thickened ear skin, scaly erythema and erythematous lesions on the back were seen and thickening of the epidermis, epidermal extension with parakeratosis were shown. These phenomena were more obvious in IL-33 treatment group(P<0.05).The expression of autophagy-related proteins in the skin lesions of the IL-33 treatment group was significantly decreased compared with the control group and IMQ group(P<0.05).Conclusions IL-33 promotes the proliferation of HaCAT cells, induces autophagy, and aggravates the occurrence and development of psoriatic lesions induced by imiquimod in mice, which may be involved in the activation of the STAT3 signaling pathway.
作者 段亚菊 王文茜 胡华 付丹丹 宋向凤 田中伟 DUAN Ya-ju;WANG Wen-qian;HU Hua;FU Dan-dan;SONG Xiang-feng;TIAN Zhong-wei(Department of Dermatology,the First Affiliated Hospital of Xinxiang Medical University,Weihui 453100;Xinxiang Medical University,Xinxiang 453003,China)
出处 《基础医学与临床》 CSCD 2020年第1期67-72,共6页 Basic and Clinical Medicine
基金 河南省卫生计生科技创新人才工程(201632) 河南省自然科学基金(162300410225) 新乡医学院研究生处创新课题(YJSCX201716Y)
关键词 白细胞介素33(IL-33) 自噬 STAT3 HACAT细胞 interleukin 33(IL-33) autophagy STAT3 HaCAT cell
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