Role of S100A8 and S100A9 in neutrophil recruitment in response to monosodium urate monohydrate crystals in the air-pouch model of acute gouty arthritis

MicroRNAs (miRNAs) are a class of noncoding RNAs that mainly negatively regulate gene expression. miRNAs have important roles in many diseases, including inflammatory diseases. Gout is a common arthritis caused by deposition of monosodium urate crystals within joints. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis. In the present review, we systemically discuss relevant publications in order to provide a better understanding on the possible role of miRNAs in gout. miRNAs may act as regulators of gout pathogenesis via several pathways. Targeting miRNAs may be a promisingstrategy in the treatment of gout.

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

Current Drug Therapy ◽

10.2174/1574885516666210719092523 ◽

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.

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Crystal-Induced Joint Disease

10.2310/im.1213 ◽

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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Treatment of acute gout

10.1093/med/9780199668847.003.0045 ◽

2016 ◽

Author(s):

Puja Khanna

Keyword(s):

Inflammatory Arthritis ◽

Adult Population ◽

Gouty Arthritis ◽

Acute Gout ◽

Monosodium Urate ◽

Epidemiological Evidence ◽

Acute Gouty Arthritis ◽

Over Time ◽

Underlying Inflammation ◽

Urate Crystals

Acute gout is a common inflammatory arthritis in the adult population. Epidemiological evidence suggests that the prevalence of gout is steadily on the rise due to longevity, coexisting comorbidities, and iatrogenic causes contributing to hyperuricaemia. Acute gout usually presents as a self-limiting flare of synovitis that occurs due to deposition of monosodium urate crystals. The frequency of flares generally increases over time in patients who continue to have hyperuricaemia and their risk factors for acute gout attacks have not been adequately addressed. Effective treatment of acute gouty arthritis is primary focused on pain which is the primary symptom but must target both the pain and underlying inflammation. Acute gout is frequently treated with non-steroidal anti-inflammatory agents, colchicine, and corticosteroids. This chapter reviews the available therapies for management of acute gout and ones that have shown promising results.

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Tu-Teng-Cao Extract Alleviates Monosodium Urate-Induced Acute Gouty Arthritis in Rats by Inhibiting Uric Acid and Inflammation

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/3095624 ◽

2020 ◽

Vol 2020 ◽

pp. 1-13

Author(s):

Rongmei Yao ◽

Zihan Geng ◽

Xin Mao ◽

Yanyan Bao ◽

Shanshan Guo ◽

...

Keyword(s):

Uric Acid ◽

Gouty Arthritis ◽

Histological Evaluation ◽

Therapeutic Effects ◽

Monosodium Urate ◽

Cell Degeneration ◽

Acute Gouty Arthritis ◽

Monosodium Urate Crystals ◽

Potassium Oxonate ◽

Urate Crystals

Gouty arthritis is an inflammatory joint disease closely related to hyperuricemia. It is characterized by deposition of monosodium urate crystals in the joints, resulting in an intense inflammatory process and pain. Control of hyperuricemia and anti-inflammation treatments are the main therapeutic approaches. However, the commonly used drugs for inhibiting uric acid and acute gouty arthritis have obvious gastrointestinal and renal toxicity; thus, there is an urgency to develop new alternative therapeutic drugs. An extract of Tu-Teng-Cao (TTC), a compound drug used in traditional Chinese medicine, has been widely applied to the clinical treatment of arthritis. In this study, we investigated the therapeutic effects of TTC on gouty arthritis. In this study, an animal model of acute gouty arthritis with hyperuricemia was established using potassium oxonate and monosodium urate crystals. After treatment with TTC, the results showed obvious therapeutic effects on the rat model of acute gouty arthritis. The treatment significantly attenuated the degree of ankle swelling, inflammation, and dysfunction index, and the levels of proinflammatory cytokines. In addition, TTC has significant antihyperuricemia activity in rats with hyperuricemia induced by potassium oxonate. Histological evaluation showed that TTC relieved pathological damage in rats with acute gouty arthritis induced by monosodium urate crystals. All the groups treated with TTC showed improvement in cartilage degeneration, cell degeneration, synovial hyperplasia, and inflammatory cell invasion in the ankle joint of rats. TTC significantly alleviated swelling, inflammation, and bleeding of the renal corpuscle and convoluted tubules of rats. The results of this study suggest that TTC is capable of treating gouty arthritis and decreasing ankle injury through the control of uric acid and inflammation.

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Trikatu, a herbal compound that suppresses monosodium urate crystal-induced inflammation in rats, an experimental model for acute gouty arthritis

Cell Biochemistry and Function ◽

10.1002/cbf.2979 ◽

2013 ◽

Vol 32 (1) ◽

pp. 106-114 ◽

Cited By ~ 13

Author(s):

Vachana Murunikkara ◽

MahaboobKhan Rasool

Keyword(s):

Experimental Model ◽

Gouty Arthritis ◽

Monosodium Urate ◽

Acute Gouty Arthritis ◽

Herbal Compound ◽

Urate Crystal

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MiR-3146 Induces Neutrophil Extracellular Traps to Aggravate Acute Gouty Arthritis

10.21203/rs.3.rs-280306/v1 ◽

2021 ◽

Author(s):

Lizhen Shan ◽

Di Yang ◽

Fabo Feng ◽

Danjie Zhu ◽

Xiaolin Li

Keyword(s):

Potential Role ◽

Gouty Arthritis ◽

Neutrophil Extracellular Traps ◽

Sirtuin 1 ◽

Luciferase Reporter ◽

Ros Production ◽

Monosodium Urate ◽

Acute Gouty Arthritis ◽

Extracellular Traps ◽

Msu Crystals

Abstract MiR-3146 plays an important role in the formation of neutrophil extracellular traps (NETs) during the pathogenesis of acute gouty arthritis (AGA).The aim of our study was to explore the underlying role and molecular mechanism of miR-3146 in the formation of neutrophil extracellular traps (NETs) during the pathogenesis of acute gouty arthritis (AGA). The expression of miR-3146 and sirtuin 1 (SIRT1) was determined by real-time PCR and western blot. The luciferase reporter assay was performed to identify the targeting relationship between miR-3146 and SIRT1. Reactive oxygen species (ROS) production was detected by fluorescent staining. NETs formation was demonstrated via immunofluorescence staining and ELISA method. AGA model was induced in rats to verify the effects of miR-3146 inhibition on histopathological changes and NETs. Here, we found miR-3146 expression was dramatically increased in neutrophils of patients with AGA, presenting higher levels of NETs. Monosodium urate (MSU) crystals significantly increased miR-3146 expression and ROS production in neutrophils. The NETs process was also triggered by MSU crystals. Furthermore, we verified the interaction between miR-3146 and SIRT1. Additionally, antagomir-3146-based therapy effectively inhibited the formation of NETs in rats with AGA. MiR-3146-mediated NETs formation may play a potential role in the pathogenesis of AGA.

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Crystal-Induced Joint Disease

10.2310/fm.1213 ◽

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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