Abstract
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.
Highlights
Gout is a metabolic disease characterized by hyperuricemia and deposition of urate crystals into the joints and accompanied by inflammatory reactions [1]
monosodium urate (MSU) crystals were synthesized with uric acid and sodium hydroxide and diluted in endotoxin-free phosphatebuffered saline (PBS) prior to injection into the right ankle joint of rats
The ankle joint and toes were significantly red and swollen, bony landmarks disappeared, and the degree of inflammation was severe (Figures 2(a) and 2(b)). ere was no inflammatory reaction in the normal group, and bony landmarks were obvious (Figure 2(c)). e ankle joints in the the effects of an extract (TTC) treatment groups were swollen; the swelling was confined to the joints without involving the toes, and the degree of inflammation was significantly lower than that noted in the model group (Figures 2(e)–2(g)). e severity of the inflammatory response was evaluated by the volume of ankle joint swelling. e volume of ankle joints was tested at 12, 24, 48, 72, and 96 h after the injection of MSU crystals
Summary
Gout is a metabolic disease characterized by hyperuricemia and deposition of urate crystals into the joints and accompanied by inflammatory reactions [1]. Is effect triggers the body’s innate immune response, leading to an induction of inflammation cascades, causing severe inflammation in the joints [8]. In the pathogenesis of acute gouty arthritis, monosodium urate (MSU) crystals are formed due to supersaturation of uric acid concentration in the joint. In this process, MSU is recognized by the resident macrophages of tissue, thereby
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