[1]姜 玥,刘宵达,吴素琴.anti-IL-33对类风湿关节炎成纤维样滑膜细胞增殖与凋亡的影响[J].医学信息,2021,34(13):81-83.[doi:10.3969/j.issn.1006-1959.2021.13.020]
 JIANG Yue,LIU Xiao-da,WU Su-qin.The Effect of anti-IL-33 on the Proliferation and Apoptosis of Fibroblast-like Synovial Cells in Rheumatoid Arthritis[J].Medical Information,2021,34(13):81-83.[doi:10.3969/j.issn.1006-1959.2021.13.020]
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anti-IL-33对类风湿关节炎成纤维样滑膜细胞增殖与凋亡的影响()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
34卷
期数:
2021年13期
页码:
81-83
栏目:
论著
出版日期:
2021-07-01

文章信息/Info

Title:
The Effect of anti-IL-33 on the Proliferation and Apoptosis of Fibroblast-like Synovial Cells in Rheumatoid Arthritis
文章编号:
1006-1959(2021)13-0081-03
作者:
姜 玥刘宵达吴素琴
(辽宁省基础医学研究所免疫研究室,辽宁 沈阳 110101)
Author(s):
JIANG YueLIU Xiao-daWU Su-qin
(Department of Immunology,Liaoning Institute of Basic Medicine,Shenyang 110101,Liaoning,China)
关键词:
anti-IL-33类风湿关节炎成纤维样滑膜细胞细胞增殖细胞凋亡
Keywords:
anti-IL-33Rheumatoid arthritis fibroblast-like synovial cellsCell proliferation Apoptosis
分类号:
R593.22
DOI:
10.3969/j.issn.1006-1959.2021.13.020
文献标志码:
A
摘要:
目的 探讨抗白细胞介素-33抗体(anti-IL-33)对类风湿关节炎(RA)成纤维样滑膜细胞(FLS)增殖与凋亡的影响及其在RA疾病中的缓解及治疗作用。方法 培养人FLS,实验分组如下:正常对照组、TNF-α(+)对照组、TNF-α(+)+anti-IL-33(50 ng/ml)组、TNF-α(+)+甲氨蝶呤(1 μg/ml)组。观察RA-FLS的形态结构,并采用CCK-8法测定各组细胞的增殖水平,流式细胞仪检测各组细胞的细胞凋亡率。结果 形态学检测显示,anti-IL-33能缓解经TNF-α处理后导致的FLS细胞变圆、间隙增加。CCK8法检测显示,与对照组比较,TNF-α(+)对照组细胞活力增加(P<0.05);与TNF-α(+)对照组比较,TNF-α(+)+anti-IL-33组和TNF-α(+)+甲氨蝶呤组细胞活力降低(P<0.05)。凋亡检测显示,与对照组比较,TNF-α(+)对照组细胞凋亡降低(P<0.05);与TNF-α(+)对照组比较,TNF-α(+)+anti-IL-33组和TNF-α(+)+甲氨蝶呤组细胞凋亡率增高(P<0.05)。结论 anti-IL-33可抑制RA-FLS增殖并诱导其凋亡,可为RA的治疗提供方向。
Abstract:
Objective To investigate the effect of anti-IL-33 antibody (anti-IL-33) on the proliferation and apoptosis of rheumatoid arthritis (RA) fibroblast-like synovial cells (FLS) and its mitigation and therapeutic effects in RA disease.Methods Cultivating human FLS, the experimental groups are as follows:Normal control group, TNF-α(+) control group, TNF-α(+) + anti-IL-33 (50 ng/ml) group, TNF-α(+) + methotrexate (1 μg/ml) group.Observing the morphology and structure of RA-FLS, and use CCK-8 method to determine the proliferation level of each group of cells, and flow cytometry to detect the apoptosis rate of each group of cells.Results Morphological examination showed that anti-IL-33 can alleviate the rounding and gap increase of FLS cells caused by TNF-α treatment.CCK8 method detection showed that compared with the control group, the cell viability of the TNF-α(+) control group increased (P<0.05);Compared with the TNF-α(+) control group, the cell viability of the TNF-α(+)+anti-IL-33 group and the TNF-α(+)+ methotrexate group were decreased (P<0.05).Apoptosis detection showed that compared with the control group, the apoptosis of the TNF-α(+) control group was reduced (P<0.05);Compared with the TNF-α(+) control group, the apoptosis rate of the TNF-α(+)+anti-IL-33 group and the TNF-α(+)+methotrexate group was increased (P<0.05).Conclusion anti-IL-33 can inhibit the proliferation of RA-FLS and induce its apoptosis, which can provide a direction for the treatment of RA.

参考文献/References:

[1]Ma JD,Jing J,Wang JW,et al.A novel function of artesunate on inhibiting migration and invasion of fibroblast-like synoviocytes from rheumatoid arthritis patients[J].Arthritis Res Ther,2019,21(1):153. [2]Kaneko S,Kondo Y,Yokosawa M,et al.Rheumatoid arthritis and cytokines[J].Nihon Rinsho,2016,74(6):913-918. [3]王鑫铭.血管紧张素Ⅱ2型受体及其信号对类风湿关节炎异常活化的滑膜巨噬细胞的调控作用[D].安徽医科大学,2019. [4]Das S,Baruah C,Saikia AK,et al.Genetic and expression changes in TNF-α as a risk factor for rheumatoid arthritis pathogenesis in northeast India[J].J Genet,2019(98):3. [5]He R,Yin H,Yuan B,et al.IL-33 improves wound healing through enhanced M2 macrophage polarization in diabetic mice[J].MolImmunol,2017(90):42-49. [6]Kashiwakura J,Yanagisawa M,Lee H,et al.Interleukin-33 Synergistically Enhances Immune Complex-Induced Tumor Necrosis Factor Alpha and Interleukin-8 Production in Cultured Human Synovium-Derived Mast Cells[J].International Archives of Allergy and Immunology,2013,161(s2):32-36. [7]Chen S,Chen B,Wen Z,et al.IL-33/ST2-mediated inflammation in macrophages is directly abrogated by IL-10 during rheumatoid arthritis[J].Oncotarget,2017,8(20):32407-32418. [8]Matsuyama Y,Okazaki H,Tamemoto H,et al.Increased levels of interleukin 33 in sera and synovial fluid from patients with active rheumatoid arthritis[J].J Rheumatol,2010(37):18-25. [9]Li Y,Fu Y,Chen H,et al.Blocking Interleukin-33 Alleviates the Joint Inflammation and Inhibits the Development of Collagen-Induced Arthritis in Mice[J].J Immunol Res,2020(2020):4297354.

更新日期/Last Update: 1900-01-01