Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (5) ◽  
pp. 1890-1898 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose Maria Fernández-Bolaños ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Autoimmune Disease ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Synovial Fibroblasts ◽  
Fibroblast Cell Line ◽  
Inflammatory Autoimmune Disease ◽  
And Oxidative Stress

Rheumatoid arthritis (RA) is a chronic and systemic inflammatory autoimmune disease mainly characterized by aggressive hyperproliferation of synovial fibroblasts (SFs).

scholarly journals Correction: Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (6) ◽  
pp. 2341-2341 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose G. Fernández-Bolaños ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Human Synovial Fibroblast ◽  
And Oxidative Stress

Correction for ‘Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982’ by Maria Luisa Castejón, et al., Food Funct., 2017, DOI: 10.1039/c7fo00210f.

scholarly journals Mechanism of miR-218-5p in autophagy, apoptosis and oxidative stress in rheumatoid arthritis synovial fibroblasts is mediated by KLF9 and JAK/STAT3 pathways

2021 ◽  
pp. jim-2020-001437
Author(s):  
Ming Chen ◽  
Minghui Li ◽  
Na Zhang ◽  
Wenwen Sun ◽  
Hui Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Signaling Pathway ◽  
Synovial Tissue ◽  
Synovial Fibroblasts ◽  
Reverse Transcription Pcr ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Interfering Rna ◽  
And Oxidative Stress

This study was aimed to investigate the effects of miR-218-5p on the proliferation, apoptosis, autophagy, and oxidative stress of rheumatoid arthritis synovial fibroblasts (RASFs), and the related mechanisms. Quantitative reverse transcription–PCR showed that the expression of miR-218-5p in rheumatoid arthritis synovial tissue was significantly higher than that in healthy synovial tissue. Compared with healthy synovial fibroblasts, miR-218-5p expression was obviously upregulated in RASFs, while KLF9 protein expression was markedly downregulated. Mechanistically, miR-218-5p could directly bind to the 3′ untranslated region of KLF9 to inhibit the expression of KLF9. Additionally, transfection of miR-218-5p small interfering RNA (siRNA) inhibited the proliferation but promoted apoptosis and autophagy of RASFs. Simultaneously, miR-218-5p silencing reduced reactive oxygen species and malondialdehyde levels and increased superoxide dismutase and glutathione peroxidase activity to improve oxidative stress in RASFs. More importantly, the introduction of KLF9 siRNA reversed the effects of miR-218-5p siRNA transfection on RASF proliferation, apoptosis, autophagy, and oxidative stress. What is more, silencing miR-218-5p inhibited the activation of JAK2/STAT3 signaling pathway by targeting KLF9. Collectively, knockdown of miR-218-5p could regulate the proliferation, apoptosis, autophagy and oxidative stress of RASFs by increasing the expression of KLF9 and inhibiting the activation of the JAK2/STAT3 signaling pathway, which may provide a potential target for the mechanism research of RA.

scholarly journals Xuebijing inhibit inflammation, oxidative stress and promote apoptosis in human synovial cells via inhibition of MEK1/2 and NF-ĸB pathway

2021 ◽  
pp. 1-9
Author(s):  
Liang Li ◽  
Yafeng Li ◽  
Da Shi ◽  
Huajian Liu ◽  
Baohui Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Cell Viability ◽  
Cell Line ◽  
Treated Group ◽  
Synovial Cells ◽  
Joint Deformity ◽  
Tnf Α ◽  
Factor Α ◽  
And Oxidative Stress

Abstract Rheumatoid arthritis (RA) is categorized as an autoimmune disease that leads to bone or joint deformity due to altered immune response. Studies have concluded the role of inflammation and oxidative stress in the progression of RA and agents inhibiting these processes showed benificial effect against the disease. Xuebijing (XBJ) injection is an intravenous patent preparation made from five-traditional Chinese medicines. Previous studies showed its excellent pharmacological activities, such as against sepsis, inflammation, and oxidative stress which has encouraged us to investigate the protective effect of XBJ against rheumatoid arthritis cell line (MH7A). For this purpose, the effect of XBJ was quantified on several parameters on the human synovial MH7A cell line activated with tumor necrosis factor-α (TNF-α). The results of the study showed that the level of tested interleukines (IL- 1β, IL- 6, IL- 8) and collagenases 1, and 13, and matrix metallo-proteinases 1, and 13 (MMP-1, and MMP-13) were found significantly reduced in XBJ treated group as compared to TNF-α treated MH7A cells. The XBJ treated group showed reduction in mRNA protein expression of COX-2 and iNOS in RT-qPCR assay. The rate of cellular apoptosis was found increased in XBJ treated group with reduction of cell viability of MH7A cells. The XBJ also showed attenuation of the expression of p-MEK/1/2 and p-p65 in MH7A cells in a western blot analysis. Our results demonstrated that XBJ significantly inhibits the inflammatory response, prevents cell viability, and induces apoptosis in human RA synovial cells by preventing the activation of the MEK/NF-κB pathway.

scholarly journals Small RNAs detected in exosomes derived from the MH7A synovial fibroblast cell line with TNF-α stimulation

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0201851 ◽  
Author(s):  
Yosuke Takamura ◽  
Wataru Aoki ◽  
Atsushi Satomura ◽  
Seiji Shibasaki ◽  
Mitsuyoshi Ueda
Keyword(s):  
Cell Line ◽  
Small Rnas ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Tnf Α

Cell-specific epigenetic drivers of pathogenesis in rheumatoid arthritis

Epigenomics ◽  
2021 ◽  
Author(s):  
Nisha Nair ◽  
Anne Barton ◽  
Anthony G Wilson
Keyword(s):  
Rheumatoid Arthritis ◽  
Autoimmune Disease ◽  
Joint Damage ◽  
Synovial Fibroblasts ◽  
Cell Types ◽  
Disease Pathogenesis ◽  
Destructive Behavior ◽  
Inflammatory Autoimmune Disease ◽  
Different Cell Types ◽  
Underlying Pathogenesis

Rheumatoid arthritis is a complex, inflammatory autoimmune disease, which is characterized by pain, swelling and joint damage driven by the altered behavior of a number of different cell types such as synovial fibroblasts macrophages and lymphocytes. The mechanism underlying pathogenesis is unclear but increasing evidence points to altered epigenetic regulation within these cell types which promotes the activated destructive behavior that underlies disease pathogenesis. This review summarizes the key epigenetic modifications in the most important cells types in rheumatoid arthritis, which are associated with disease activity. We also discuss emerging avenues of research focusing on readers of epigenetic markers which may serve to be potential therapeutic targets.

scholarly journals Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 45
Author(s):  
Helena Beatriz Ferreira ◽  
Tânia Melo ◽  
Artur Paiva ◽  
Maria do Rosário Domingues
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Profile ◽  
Inflammatory Responses ◽  
Molecular Level ◽  
Lipid Hydroperoxides ◽  
Lipid Species ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

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