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白细胞介素-37(IL-37)抑制百日咳毒素诱导的大鼠炎性肌病。

Interleukin-37 (IL-37) Suppresses Pertussis Toxin-Induced Inflammatory Myopathy in a Rat Model.

机构信息

Department of Rheumatology, Qilu Hospital of Shandong University, Ji'nan, Shandong, China (mainland).

Department of Rheumatology and Immunology, Linyi People's Hospital, Linyi, Shandong, China (mainland).

出版信息

Med Sci Monit. 2018 Dec 18;24:9187-9195. doi: 10.12659/MSM.910904.

Abstract

BACKGROUND Recent data have demonstrated the potential immunosuppressive roles of interleukin-37 (IL-37) in several diseases, but whether it is involved in the pathogenesis of inflammatory myopathy has not been elucidated. MATERIAL AND METHODS An experimental autoimmune myositis (EAM) model was built by subcutaneous injections of pertussis toxin (PTX) and purified rabbit myosin (10mg/kg) emulsified with an equal volume of conventional complete Freund's adjuvant (CFA) in a Lewis model. Autoimmune myositis Lewis model rats were divided into 3 groups: group A rats (control group) were injected with CFA in saline weekly; group B (IL-37 group) rats were injected with saline with IL-37 and CFA in saline weekly; and group C (IL-37 + SIS3 group) rats were injected with IL-37, CFA, and SIS3. ELISA was also used to assess the expressions of TNF-α, IL-6, IL-1β, TGF-β1, and CK. HE staining was performed to assess pathological changes in lung and muscle tissues. RESULTS The expressions of TNF-α, IL-6, IL-1β, TGF-β1, and CK significantly increased in autoimmune myositis Lewis model rats. After IL-37 treatment, the expression of TNF-α, IL-6, IL-1β, TGF-β1, and CK was significantly reduced, as were the inflammatory responses of lung and muscle. However, SIS3 reduced the effects of IL-37 on the autoimmune myositis Lewis model rats. CONCLUSIONS These findings indicate that IL-37 protects against inflammatory response via regulating Smad3 in autoimmune myositis Lewis model rats.

摘要

背景

最近的数据表明白细胞介素-37(IL-37)在几种疾病中具有潜在的免疫抑制作用,但它是否参与炎症性肌病的发病机制尚未阐明。

材料和方法

通过皮下注射百日咳毒素(PTX)和纯化的兔肌球蛋白(10mg/kg)与等体积的常规完全弗氏佐剂(CFA)在 Lewis 模型中乳化,建立实验性自身免疫性肌炎(EAM)模型。将自身免疫性肌炎 Lewis 模型大鼠分为 3 组:A 组(对照组)每周用 CFA 生理盐水注射;B 组(IL-37 组)大鼠每周用 IL-37 和 CFA 生理盐水注射;C 组(IL-37+SIS3 组)大鼠注射 IL-37、CFA 和 SIS3。ELISA 还用于评估 TNF-α、IL-6、IL-1β、TGF-β1 和 CK 的表达。进行 HE 染色以评估肺和肌肉组织的病理变化。

结果

自身免疫性肌炎 Lewis 模型大鼠 TNF-α、IL-6、IL-1β、TGF-β1 和 CK 的表达显著增加。IL-37 治疗后,TNF-α、IL-6、IL-1β、TGF-β1 和 CK 的表达明显降低,肺和肌肉的炎症反应也减轻。然而,SIS3 降低了 IL-37 对自身免疫性肌炎 Lewis 模型大鼠的作用。

结论

这些发现表明,IL-37 通过调节 Smad3 来保护自身免疫性肌炎 Lewis 模型大鼠免受炎症反应的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1874/6322374/84ca85dfe5b8/medscimonit-24-9187-g001.jpg

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