scholarly journals Total glucosides of paeony protects THP-1 macrophages against monosodium urate-induced inflammation via MALAT1/miR-876-5p/NLRP3 signaling cascade in gouty arthritis

2021 ◽  
Vol 138 ◽  
pp. 111413 ◽  
Author(s):  
Qingliang Meng ◽  
Wanting Meng ◽  
Hua Bian ◽  
Fuzeng Zheng ◽  
Huimin Gu ◽  
...  
Keyword(s):  
Gouty Arthritis ◽  
Signaling Cascade ◽  
Monosodium Urate ◽  
Total Glucosides Of Paeony

Biostatistical Analysis and Possible Forecasting of Relationship Between Uric Acid and Specific Laboratory Tests in Cases of Gouty Arthritis

2017 ◽  
Vol 68 (6) ◽  
pp. 1234-1241
Author(s):  
Adina Octavia Duse ◽  
Delia Berceanu Vaduva ◽  
Mirela Nicolov ◽  
Cristina Trandafirescu ◽  
Marcel Berceanu Vaduva ◽  
...  
Keyword(s):  
Uric Acid ◽  
Laboratory Tests ◽  
Gouty Arthritis ◽  
Main Diagnosis ◽  
Monosodium Urate ◽  
Glutamate Pyruvate ◽  
Metatarsophalangeal Joints ◽  
The Relationship ◽  
Biostatistical Analysis ◽  
Urate Crystals

Acute gouty arthritis represents an inflammatory response to microcrystals of monosodium urate that precipitate in joint tissues from supersaturated body fluids or are shed from preexisting articular deposits [1]. Gout is a metabolic disease characterized by recurrent episodes of arthritis associated with the presence of monosodium urate crystals in the tissue or synovial fluid during the attack.These forms of crystal-induced arthritis usually affect peripheral joints, including knee, ankle, wrist, and metacarpophalangeal and metatarsophalangeal joints. All of them may be associated with other inflammatory, endocrine diseases [2]. The present study was done to highlight the relationship between increased levels of uric acid and specific laboratory tests in order to possible forecast development of further disease in patients with gouty arthrithis.The present study was done on 34 patients hospitalized in Felix Hospital of Rehabilitation in 2015-2016, with age between 44 and 74, having the main diagnosis of gouty arthritis.We studied the following laboratory tests:urea and other related analysis, like uric acid, creatinine, cholesterol, glutamate pyruvate transaminase and glutamate oxalate transaminase.

scholarly journals Autoinflammatory Features in Gouty Arthritis

2021 ◽  
Vol 10 (9) ◽  
pp. 1880
Author(s):  
Paola Galozzi ◽  
Sara Bindoli ◽  
Andrea Doria ◽  
Francesca Oliviero ◽  
Paolo Sfriso
Keyword(s):  
Differential Diagnosis ◽  
Inflammatory Arthritis ◽  
Important Implication ◽  
Gouty Arthritis ◽  
Molecular Genetic ◽  
Therapeutic Options ◽  
Monosodium Urate ◽  
Inflammatory Pathways ◽  
Genetic Contributions

In the panorama of inflammatory arthritis, gout is the most common and studied disease. It is known that hyperuricemia and monosodium urate (MSU) crystal-induced inflammation provoke crystal deposits in joints. However, since hyperuricemia alone is not sufficient to develop gout, molecular-genetic contributions are necessary to better clinically frame the disease. Herein, we review the autoinflammatory features of gout, from clinical challenges and differential diagnosis, to the autoinflammatory mechanisms, providing also emerging therapeutic options available for targeting the main inflammatory pathways involved in gout pathogenesis. This has important implication as treating the autoinflammatory aspects and not only the dysmetabolic side of gout may provide an effective and safer alternative for patients even in the prevention of possible gouty attacks.

Ozone Therapy Alleviates Monosodium Urate Induced Acute Gouty Arthritis in Rats Through Inhibition of NLRP3 Inflammasome

2021 ◽  
Vol 16 ◽  
Author(s):  
Doaa M. Abdullah ◽  
Soad L. Kabil
Keyword(s):  
Gouty Arthritis ◽  
Antioxidant Defense System ◽  
Albino Rats ◽  
Monosodium Urate ◽  
Ozone Therapy ◽  
Reference Drug ◽  
Acute Gouty Arthritis ◽  
Beneficial Effects ◽  
Anti Inflammatory ◽  
Domain 3

Background: Gout is a metabolic disease strictly related to hyperuricemia. The associated intense inflammation and pain are triggered by the deposited monosodium urate crystals (MSU) in joints. The principal therapeutic strategies of gout involve the control of hyperuricemia and anti-inflammatory medications. Objectives: This study aimed to investigate the possible beneficial effects of ozone therapy, a well-known antioxidant, and an immunomodulation, on gouty arthritis and the underlying mechanisms. Methods : Acute gouty arthritis was induced in male albino rats via MSU crystals intra-articular injection in the ankle joint. The gouty arthritic rats received pre-treatment with ozone, colchicine (as a reference drug), or combination. Results : The obtained results of ozone therapy showed obvious reduction in the degree of ankle edematous swelling, pro-inflammatory cytokines, lipid peroxidation, the nucleotide binding oligomerization domain like receptor containing pyrin domain 3 (NLRP3), procaspase-1, caspase-1, interleukin-1β synovial tissue levels with enhancement of antioxidant defense system. Additionally, ozone therapy significantly attenuated the histological derangements in gouty arthritic rats. Conclusion : This study suggests that ozone is able to treat gouty arthritis and reducing synovial injury through an anti-inflammatory effect as well as antioxidant activity.

scholarly journals Cichoric Acid Ameliorates Monosodium Urate-Induced Inflammatory Response by Reducing NLRP3 Inflammasome Activation via Inhibition of NF-kB Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qi Wang ◽  
Bingfeng Lin ◽  
Zhifeng Li ◽  
Jie Su ◽  
Yulin Feng
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
Gouty Arthritis ◽  
Inflammasome Activation ◽  
Cichoric Acid ◽  
Monosodium Urate ◽  
Protein Levels ◽  
Nlrp3 Inflammasome Activation ◽  
Tnf Α

Gouty arthritis is characterized by the deposition of monosodium urate (MSU) within synovial joints and tissues due to increased urate concentrations. Here, we elucidated the role of the natural compound cichoric acid (CA) on the MSU crystal-stimulated inflammatory response. The THP-1-derived macrophages (THP-Ms) were pretreated with CA and then stimulated with MSU suspensions. The protein levels of p65 and IκBα, the activation of the NF-κB signaling pathway by measuring the expression of its downstream inflammatory cytokines, and the activity of NLRP3 inflammasome were measured by western blotting and ELISA. CA treatment markedly inhibited the degradation of IκBα and the activation of NF-κB signaling pathway and reduced the levels of its downstream inflammatory genes such as IL-1β, TNF-α, COX-2, and PGE2 in the MSU-stimulated THP-M cells. Therefore, we infer that CA effectively alleviated MSU-induced inflammation by suppressing the degradation of IκBα, thereby reducing the activation of the NF-κB signaling pathway and the NLRP3 inflammasome. These results suggest that CA could be a novel therapeutic strategy in averting acute episodes of gout.

scholarly journals Zisheng Shenqi Decoction Ameliorates Monosodium Urate-Mediated Gouty Arthritis in Rats via Promotion of Autophagy through the AMPK/mTOR Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jieru Han ◽  
Guangyu Shi ◽  
Wenhao Li ◽  
Shuhui Wang ◽  
Jixiang Bai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Gouty Arthritis ◽  
Nitrogen Monoxide ◽  
Joint Space ◽  
Mtor Signaling ◽  
Receptor Protein ◽  
Related Factor ◽  
Monosodium Urate ◽  
Mtor Signaling Pathway

Gouty arthritis (GA) is an inflammatory disease owing to the accumulation of monosodium urate (MSU) in joints, leading to redness and burning pain. In this study, the effect of Zisheng Shenqi Decoction (ZSD) on a rat model of MSU-induced GA was investigated. ZSD obviously diminished the right paw thickness, the degree of the swelling of the paw, and the infiltration of the inflammatory cell, as well as cartilage erosion, and widened the joint space in MSU-treated rats. Besides, MSU remarkably elevated the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-18; however, ZSD treatment dose dependently lowered these levels and resulted in a significant decrease in articular elastase activity. Also, ZSD administration increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) but declined malondialdehyde (MDA) and nitrogen monoxide (NO) contents. Importantly, western blotting analysis revealed that NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, IL-1β, nuclear factor-E2-related factor 2 (Nrf2) in the cytoplasm, phosphorylated mammalian target of rapamyclin (p-mTOR), and p62 expressions were downregulated, whereas the levels of nuclear Nrf2, phosphorylated AMP-activated protein kinase (p-AMPK), Beclin-1, and LC3II/I were upregulated by ZSD. Immunofluorescence assay indicated that ZSD evidently promoted nuclear translocation of LC3. Taken together, ZSD inhibited inflammation and oxidative stress and facilitated autophagy through the activation of the AMPK pathway and suppression of the mTOR signaling pathway, demonstrating its potential for preventing and curing GA.

scholarly journals 724 Evaluation of an anti-human IL-1β antibody in monosodium urate crystals-induced peritonitis model in hIL-1β HuGEMM™ mice

2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A753-A753
Author(s):  
Xiaoyu An ◽  
Kaixia Lian ◽  
Jia Zheng ◽  
Fei Jian ◽  
Henry Li ◽  
...  
Keyword(s):  
Treatment Group ◽  
Murine Model ◽  
Gouty Arthritis ◽  
Chronic Inflammatory Disease ◽  
Vehicle Group ◽  
Inflammasome Activation ◽  
Monosodium Urate ◽  
Vehicle Treatment ◽  
Peritonitis Model ◽  
Msu Crystals

BackgroundGout is a chronic inflammatory disease featuring the deposition of monosodium urate (MSU) crystals in the synovial fluid of patients, followed by NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome activation and bioactive IL-1β release, which recruits neutrophils to the local inflammation sites. Blocking IL-1β function is becoming a a potent therapeutic approach for gout and gouty arthritis. Conventional MSU-induced peritonitis in C57BL/6 mice provides a simple and rapid evaluation of therapeutics targeting inflammasome activation. However, this murine model has limitations when it comes to the evaluation of human-specific antibodies, for example, anti-human IL-1β (anti-hIL-1β) monoclonal antibodies (mAb). Thus, a murine model to assess the efficacy of anti-hIL-1β mAb is needed. We have developed a hIL-1β knock-in mouse model (hIL-1β HuGEMM™), which is able to facilitate the pre-clinical evaluation of drugs targeting specific human biological molecules especially when mouse ortholog is not available. Therefore, an MSU crystals induced peritonitis model using hIL-1β HuGEMM™ mice provides a robust model to evaluate therapies targeting hIL-1β.MethodsMSU crystals were injected intraperitoneally into human IL-1β (hIL-1β) knock-in mice, where the coding sequence of mouse IL-1β was replaced by hIL-1β. Prior to MSU crystal administration, mice received treatment of either vehicle or anti-hIL-1β antibody. Six hours facilitate post MSU crystal injection, serum and lavage flushed with PBS were collected. Subsequently, cytokine protein levels in the serum were determined by MSD, and the population of polymorphonuclear leukocytes (PMNs) (live CD11b+ Ly-6GHi cells) in the lavage was analysed by flow cytometry.ResultsThe vehicle treatment group showed a dramatic increase in hIL-1β secretion and PMN leukocytes, in comparison to the group that did not receive MSU, which suggests a successful induction of acute inflammatory response in the peritoneal cavity. In contrast, mice that received a single administration of anti-hIL-1β antibody 24 hours prior to MSU injection exhibited a significantly lower level of hIL-1β when compared to the vehicle treatment group, which implies that the anti-hIL-1β mAb efficaciously neutralized hIL-1β secretion. In addition, TNF-α and IL-6, two further cytokines downstream of IL-1β, were significantly reduced in the anti-hIL-1β mAb treatment group. However, the PMN leukocyte infiltration in the anti-hIL-1β mAb treatment group did not change in comparison to the vehicle group.ConclusionsIn this study, an MSU crystals-induced peritonitis model was successfully established in hIL-1β HuGEMM mice, which has the potential to evaluate immune therapeutics with anti-hIL-1β blockades.

scholarly journals Hyperuricemia and Gout – Ins and Out

2020 ◽  
Vol 15 (2) ◽  
pp. 227-234
Author(s):  
Md Abdur Razzak ◽  
Quazi Audry Arafat Rahman ◽  
Fahtiha Nasreen
Keyword(s):  
Gouty Arthritis ◽  
Polarized Light ◽  
Acute Gout ◽  
Women Patients ◽  
Monosodium Urate ◽  
Tophaceous Gout ◽  
First Metatarsal ◽  
Birefringent Crystals ◽  
Inflammatory Drugs ◽  
Urate Crystals

Gout is a condition characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout. The peak incidence occurs in patients 30 to 50 years old, and the condition is much more common in men than in women. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle. Acute gout most commonly affects the first metatarsal joint of the foot, but other joints are also commonly involved. Definitive diagnosis requires joint aspiration with demonstration of birefringent crystals in the synovial fluid under a polarized light microscope. Treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, corticosteroids and analgesics. In patients without complications, NSAID therapy is preferred. JAFMC Bangladesh. Vol 15, No 2 (December) 2019: 227-234

Crystal-Induced Joint Disease

2019 ◽  
Author(s):  
N Lawrence Edwards
Keyword(s):  
Inflammatory Arthritis ◽  
Gouty Arthritis ◽  
Clinical Manifestations ◽  
Calcium Pyrophosphate ◽  
Calcium Pyrophosphate Dihydrate ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Acute Gouty Arthritis ◽  
Crystal Arthritis ◽  
Pyrophosphate Dihydrate

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis

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