血红素加氧酶 1 在类风湿关节炎和 IL-1 诱导的炎症细胞模型中的作用

IF 1.1 4区 医学 Q4 MEDICAL LABORATORY TECHNOLOGY
Mingshan Li, Nan Zheng
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引用次数: 0

摘要

目的:类风湿性关节炎(RA)是一种常见的慢性自身免疫性炎症:类风湿性关节炎(RA)是一种常见的慢性自身免疫性炎症疾病。类风湿性关节炎的发病机制复杂,缺乏有效的治疗药物。研究发现,血红素加氧酶 1(HO-1)在 RA 中会减少。然而,HO-1在RA中的作用及相关机制尚未阐明:方法:建立 RA 大鼠模型。方法:建立 RA 大鼠模型。分析体重增加率、脚趾肿胀程度和关节炎指数,以评估 HO-1 对 RA 的治疗效果。使用 5 ng/mL IL-1 建立体外 RAW264.7 炎症细胞模型。用SnPP或hemin抑制或上调HO-1的表达。选择四唑盐比色法(MTT)检测细胞增殖。ELISA 用于测定细胞炎症因子 IL-1 和 IL-6 的浓度。评估了活性氧(ROS)活性。通过 Western 印迹分析 NF-[式中:见正文]B 和 MMP-3 的表达:结果:HO-1在RA大鼠中的表达量减少,而hemin可提高关节炎大鼠的HO-1水平,从而提高体重增加率,降低脚趾肿胀程度和关节炎指数(PPP结论:HO-1的上调可改善RA大鼠的关节炎症状:上调HO-1可通过减少ROS表达、抑制NF-[配 方:见正文]B信号通路、提高MMP-3表达、减少炎性因子分泌、抑制炎性细胞增殖等作用改善关节炎症状。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of Heme Oxygenase 1 in Rheumatoid Arthritis and IL-1 Induced Inflammatory Cell Model.

Objective: Rheumatoid arthritis (RA) is a common chronic autoimmune inflammatory disease. The pathogenesis of RA is complex, and RA lacks effective therapeutic drugs. Heme oxygenase 1 (HO-1) is found to be reduced in RA. However, the role of HO-1 in RA and related mechanisms have not been elucidated.

Methods: RA rat model was established. The expression of HO-1 was upregulated by hemin. The increase weight rate, the degree of toe swelling, and the arthritis index were analyzed to evaluate the therapeutic effect of HO-1 on RA. In vitro RAW264.7 inflammatory cell model was established using 5 ng/mL IL-1. SnPP or hemin were used to inhibit or upregulate HO-1 expression. Tetrazolium salt colorimetric assay (MTT) was selected to test cell proliferation. ELISA was used to determine the concentrations of cellular inflammatory factors IL-1 and IL-6. Reactive oxygen species (ROS) activity was assessed. Western blot was performed to analyze NF-[Formula: see text]B and MMP-3 expressions.

Results: The expression of HO-1 was decreased in RA rats, and hemin increased HO-1 level in arthritic rats, which elevated the increase weight rate and decreased toe swelling degree and arthritis index (P<0.05). Hemin significantly upregulated HO-1 expression, inhibited inflammatory cell proliferation, decreased IL-1 and IL-6 expressions, declined ROS level, restrained NF-[Formula: see text]B expression, and enhanced MMP-3 expression in Raw264.7 cells induced by LPS (P<0.05). SnPP obviously inhibited the expression of HO-1, promoted cell proliferation, elevated IL-1 and IL-6 secretions, increased ROS level, promoted NF-[Formula: see text]B expression, and decreased MMP-3 level compared with LPS group (P<0.05).

Conclusion: Upregulation of HO-1 can improve arthritis symptoms by reducing ROS expression, inhibiting NF-[Formula: see text]B signaling pathway, elevating MMP-3 expression, attenuating inflammatory factor secretion, and suppressing inflammatory cell proliferation.

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来源期刊
Annals of clinical and laboratory science
Annals of clinical and laboratory science 医学-医学实验技术
CiteScore
1.60
自引率
0.00%
发文量
112
审稿时长
6-12 weeks
期刊介绍: The Annals of Clinical & Laboratory Science welcomes manuscripts that report research in clinical science, including pathology, clinical chemistry, biotechnology, molecular biology, cytogenetics, microbiology, immunology, hematology, transfusion medicine, organ and tissue transplantation, therapeutics, toxicology, and clinical informatics.
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