Plasma and Synovial Levels of Tolmetin and Its Inhibitory Effect on Prostaglandins in Patients with Rheumatoid Arthritis

2015 ◽  
pp. 167-172
Author(s):  
I. Caruso ◽  
M. Tirrito ◽  
S. Santandrea ◽  
F. Nitti ◽  
M. Greco ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inhibitory Effect

scholarly journals The Inhibitory Effect of IFN-γ on Protease HTRA1 Expression in Rheumatoid Arthritis

2014 ◽  
Vol 193 (1) ◽  
pp. 130-138 ◽  
Author(s):  
Yuzhu Hou ◽  
Haijiang Lin ◽  
Linnan Zhu ◽  
Zhaoting Liu ◽  
Fanlei Hu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inhibitory Effect ◽  
Ifn Γ

scholarly journals Inhibitory Effect of a Novel Antirheumatic Drug T-614 on the IL-6-Induced RANKL/OPG, IL-17, and MMP-3 Expression in Synovial Fibroblasts from Rheumatoid Arthritis Patients

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yu Wei ◽  
Xiaoxun Sun ◽  
Minhui Hua ◽  
Wenfeng Tan ◽  
Fang Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
Inhibitory Effect ◽  
Antirheumatic Drug ◽  
Orphan Receptor ◽  
Rankl Expression ◽  
Articular Damage ◽  
Receptor Activator

T-614 (also named as iguratimod), a novel antirheumatic drug, could attenuate joint inflammation and articular damage in rheumatoid arthritis (RA) patients, providing a new therapy for RA. Here, we tested the role T-614 on the IL-6-induced receptor activator of nuclear factorκB ligand (RANKL)/osteoprotegerin (OPG), IL-17, and MMP-3 expression in synovial fibroblasts from rheumatoid arthritis (RASFs) patients. T-614 decreased RANKL expression and RANKL/OPG ratio in IL-6-induced RASFs. We confirmed this effect by a decrease of the mRNA and protein RANKL and mRNA RANKL/OPG in RASFs exposed in vitro to T-614 or MTX. Markedly decreased levels of IL-17, retinoid-related orphan receptor C (RORc), and MMP-3 mRNA expression were also observed in IL-6-induced RASFs in the presence of T-614 or MTX compared with those in its absence. Furthermore, T-614 blocked expression of p-ERK1/2 protein without affecting ERK1/2 expression, indicating that the way that T-614 regulated RANKL expression might be ERK1/2 pathway. Our results suggest that T-614 yields a strong improvement in arthritis via exact suppression of RANKL/OPG, IL-17, and MMP-3 expression in RASFs.

scholarly journals Different Original and Biosimilar TNF Inhibitors Similarly Reduce Joint Destruction in Rheumatoid Arthritis—A Network Meta-Analysis of 36 Randomized Controlled Trials

2019 ◽  
Vol 20 (18) ◽  
pp. 4350 ◽  
Author(s):  
Niels Graudal ◽  
Benjamin Skov Kaas-Hansen ◽  
Louise Guski ◽  
Thorbjørn Hubeck-Graudal ◽  
Nicky J. Welton ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Randomized Controlled Trials ◽  
Meta Analysis ◽  
Joint Destruction ◽  
Inhibitory Effect ◽  
Placebo Control ◽  
Controlled Trials ◽  
Randomized Controlled ◽  
High Doses ◽  
Necrosis Factor

The effect of five approved tumour necrosis factor inhibitors (TNFi: infliximab, etanercept, adalimumab, certolizumab, and golimumab) on joint destruction in rheumatoid arthritis (RA) have been compared versus methotrexate (MTX) in randomized controlled trials (RCTs) but have not been compared directly to each other or to an otherwise untreated placebo control. The present analysis compares effects of standard doses, high doses, and low doses of TNFis on radiographic joint destruction in RA and relate these effects to MTX and placebo by means of a Bayesian network meta-analysis. We identified 31 RCTs of the effect of TNFis on joint destruction and 5 RCTs with controls, which indirectly could link otherwise untreated placebo controls to the TNFi treatments in the network. The previously untested comparison with placebo was performed to estimate not only the effect relative to another drug, but also the absolute attainable effect. Compared to placebo there was a highly significant inhibitory effect on joint destruction of infliximab, etanercept, adalimumab, certolizumab, and golimumab, which was about 0.9% per year as monotherapy and about 1.2% per year when combined with MTX. Although significantly better than MTX and placebo, golimumab seemed inferior to the remaining TNFis. There was no difference between original reference drugs (Remicade, Enbrel) and the almost identical copy drugs (biosimilars).

Abstract 305: HDL Antagonizes the Defects in the Lymphatic System that Contribute to the Pathogenesis of Rheumatoid Arthritis

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Radjesh Bisoendial ◽  
Wolfgang Weninger ◽  
Francine Petrides ◽  
Fatiha Tabet ◽  
Paul P Tak ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Tube Formation ◽  
Mrna Levels ◽  
Long Term Effects ◽  
Hypoxic Conditions ◽  
Therapeutic Benefits ◽  
Erosive Arthropathy

Rheumatoid arthritis (RA) is a common inflammatory erosive arthropathy that increases cardiovascular (CV) risk two-fold. Lymphatic dysfunction, a hallmark of chronic inflammation, is considered an attractive target to resolve synovial inflammation. Given the strong vascular anti-inflammatory properties of high-density lipoprotein (HDL) and its key apolipoprotein (apo)A-I, we hypothesized that they may promote inflammation resolution in RA by improving lymphatic endothelial function via up-regulation of the homeobox-containing transcription factor, Prox-1,a key regulator of inflammation-induced lymphangiogenesis (IIL) . Primary human dermal lymphatic endothelial cells (LEC) were treated for 3 days with TNFα (10 ng/mL) or pre-incubated with apoA-I (1.2 mg/mL) for 24 h, followed by TNFα exposure for 3 days. Prox1 mRNA levels were quantified by qPCR. For the tube formation assay, LECs were seeded into a pre-coated Matrigel 24-well plate, and treated with TNFα for 6 h or pre-incubated with apoA-I for 24 h, followed by TNFα exposure for 6 h. Mouse thoracic ducts (TD) were isolated from 2-4 month old C57Bl/6 mice for studying lymphatic vessel (LV) sprouting. TD rings (1 mm) were implanted into a 3-D culture system containing Matrigel under hypoxic conditions and either treated with TNFα, or pre-incubated for 24 h with apoA-I then exposed to TNFα. Incubation with TNFα decreased LEC Prox1 mRNA levels by about 56% (P<0.05). Prior exposure of LECs to apoA-I blocked TNFα-mediated Prox-1 suppression (P<0.05). TNFα also reduced LEC tube formation by about 55% (p<0.05) and completely inhibited LV sprouting from TD rings (p<0.05). ApoA-I protected against TNFα-mediated inhibition of LEC tube formation (44.7±8.1 versus 81.9±15.0% of control; P<0.05) and the inhibitory effect of TNFα on LV sprouting (P<0.05). These results suggest that apoA-I directly regulates IIL by upregulating Prox1 and protecting against TNFα-mediated restriction of lymphatic sprouting and growth in vitro. Hence, raising HDL may provide dual therapeutic benefits in RA by targeting inflammation and reducing cardiovascular risk. New classes of HDL-raising drugs will allow us to study the long term effects of increasing HDL levels on RA progression and CV risk.

Plasma and Synovial Fluid Pharmacokinetics and Prostaglandin Inhibitory Effect of Indoprofen in Patients with Rheumatoid Arthritis

1980 ◽  
Vol 9 (2) ◽  
pp. 123-126 ◽  
Author(s):  
Innocenzo Caruso ◽  
Enzo Moro ◽  
Carlo Patrono ◽  
Gabriele Sacchetti ◽  
Vittore Tamassia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Inhibitory Effect

scholarly journals Inhibitory Effect ofChrysanthemum zawadskiiHerbich var.latilobumKitamura Extract on RANKL-Induced Osteoclast Differentiation

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Dong Ryun Gu ◽  
Jin-Ki Hwang ◽  
Munkhsoyol Erkhembaatar ◽  
Kang-Beom Kwon ◽  
Min Seuk Kim ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Diseases ◽  
Osteoclast Differentiation ◽  
Ethanol Extract ◽  
Inhibitory Effect ◽  
Bone Diseases ◽  
Dependent Manner ◽  
Erk Activation

Chrysanthemum zawadskii Herbichvar.latilobum Kitamura, known as “Gujulcho” in Korea, has been used in traditional medicine to treat various inflammatory diseases, including rheumatoid arthritis. However, these effects have not been tested on osteoclasts, the bone resorbing cells that regulate bone metabolism. Here, we investigated the effects ofC. zawadskiiHerbich var.latilobumKitamura ethanol extract (CZE) on osteoclast differentiation induced by treatment with the receptor activator of NF-κB ligand (RANKL). CZE inhibited osteoclast differentiation and formation in a dose-dependent manner. The inhibitory effect of CZE on osteoclastogenesis was due to the suppression of ERK activation and the ablation of RANKL-stimulated Ca2+-oscillation via the inactivation of PLCγ2, followed by the inhibition of CREB activation. These inhibitory effects of CZE resulted in a significant repression of c-Fos expression and a subsequent reduction of NFATc1, a key transcription factor for osteoclast differentiation, fusion, and activationin vitroandin vivo. These results indicate that CZE negatively regulates osteoclast differentiation and may be a therapeutic candidate for the treatment of various bone diseases, such as postmenopausal osteoporosis, rheumatoid arthritis, and periodontitis.

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