scholarly journals Sodium hyaluronate inhibits interleukin-1-evoked reactive oxygen species of bovine articular chondrocytes

2001 ◽  
Vol 9 (4) ◽  
pp. 390-392 ◽  
Author(s):  
K. Fukuda ◽  
M. Oh ◽  
S. Asada ◽  
F. Hara ◽  
M. Matsukawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Articular Chondrocytes ◽  
Interleukin 1 ◽  
Sodium Hyaluronate ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bovine Articular Chondrocytes

scholarly journals Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species

2001 ◽  
Vol 10 (4) ◽  
pp. 209-215 ◽  
Author(s):  
A. Ferreira Mendes ◽  
A. Pato Carvalho ◽  
M. Margarida Caramona ◽  
M. Celeste Lopes
Keyword(s):  
Reactive Oxygen Species ◽  
Articular Chondrocytes ◽  
Reactive Oxygen ◽  
Inos Expression ◽  
Inos Mrna ◽  
No Production ◽  
Dependent Manner ◽  
Ros Production ◽  
Oxygen Species ◽  
Bovine Articular Chondrocytes

Aims:In this work, we studied the mechanisms by which diphenyleneiodonium chloride (DPI) inhibits nitric oxide (NO) synthesis induced by the pro-inflammatory cytokine interleukin-1β (IL-1) in bovine articular chondrocytes. To achieve this, we evaluated the ability of DPI to inhibit the expression and activity of the inducible isoform of the NO synthase (iNOS) induced by IL-1. We also studied the ability of DPI to prevent IL-1-induced NF-κB activation and reactive oxygen species (ROS) production.Results:Northern and Western blot analysis, respectively, showed that DPI dose-dependently inhibited IL-1-induced iNOS mRNA and protein synthesis in primary cultures of bovine articular chondrocytes. DPI effectively inhibited NO production (IC50= 0.03 Ī 0.004 μ M), as evaluated by the method of Griess. Nuclear factor-kappa B (NF- κB) activation, as evaluated by electrophoretic mobility shift assay, was inhibited by DPI (1-10 μ M) in a dose-dependent manner. IL-1-induced ROS production, as evaluated by measurement of dichlorofluorescein fluorescence, was inhibited by DPI at concentrations that also prevented NF-κB activation and iNOS expression.Conclusions:DPI inhibits IL-1-induced NO production in chondrocytes by two distinct mechanisms: (i) by inhibiting NOS activity, and (ii) by preventing iNOS expression through the blockade of NF-κB activation. These results also support the involvement of reactive oxygen species in IL-1-induced NF-κB activation and expression of NF-κB-dependent genes, such as iNOS.

scholarly journals Decoy Receptor 3 Promotes Preosteoclast Cell Death via Reactive Oxygen Species-Induced Fas Ligand Expression and the IL-1α/IL-1 Receptor Antagonist Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yi-Jen Peng ◽  
Ching-Tsung Peng ◽  
Yi-Hsuan Lin ◽  
Gu-Jiun Lin ◽  
Shing-Hwa Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Resorption ◽  
Fas Ligand ◽  
Interleukin 1 ◽  
Reactive Oxygen ◽  
Precursor Cells ◽  
Osteoclast Precursor ◽  
Oxygen Species ◽  
Decoy Receptor ◽  
Decoy Receptor 3

Purpose. Interleukin-1α (IL-1α) is a potent cytokine that plays a role in inflammatory arthritis and bone loss. Decoy receptor 3 (DCR3) is an immune modulator of monocytes and macrophages. The aim of this study was to investigate the mechanism of DCR3 in IL-1α-induced osteoclastogenesis. Methods. We treated murine macrophages with DCR3 during receptor activator of nuclear factor kappa Β ligand- (RANKL-) plus IL-1α-induced osteoclastogenesis to monitor osteoclast formation by tartrate-resistant acid phosphatase (TRAP) staining. Osteoclast activity was assessed using a pit formation assay. The mechanisms of inhibition were studied by biochemical analyses, including RT-PCR, immunofluorescent staining, flow cytometry, an apoptosis assay, immunoblotting, and ELISA. Results. DCR3 suppresses IL-1α-induced osteoclastogenesis in both primary murine bone marrow-derived macrophages (BMM) and RAW264.7 cells as it inhibits bone resorption. DCR3 induces RANKL-treated osteoclast precursor cells to express IL-1α, secretory IL-1ra (sIL-1ra), intracellular IL-1ra (icIL-1ra), reactive oxygen species (ROS), and Fas ligand and to activate IL-1α-induced interleukin-1 receptor-associated kinase 4 (IRAK4). The suppression of DCR3 during RANKL- or IL-1α-induced osteoclastogenesis may be due to the abundant secretion of IL-1ra, accumulation of ROS, and expression of Fas ligand in apoptotic osteoclast precursor cells. Conclusions. We concluded that there is an inhibitory effect of DCR3 on osteoclastogenesis via ROS accumulation and ROS-induced Fas ligand, IL-1α, and IL-1ra expression. Our results suggested that the upregulation of DCR3 in preosteoclasts might be a therapeutic target in inflammatory IL-1α-induced bone resorption.

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