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https://www.selleckchem.com/products/rki-1447.html The efficacy of drug usage was determined based on the survival rate after drug administration. The most efficient drugs, drug combinations, and their mechanism of action were discussed in regard to the present recommendations for the treatment of GAE, EDA, BAE, and PAM. At the end, this review aims to provide a useful tool for physicians in their choice to optimize the treatment of FLA infections. MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR-223-3p and miR-22-3p in gouty-associated inflammation. In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual-luciferase reporter assay was used to verify the direct target of miR-223-3p and miR-22-3p. We found that miR-223-3p and miR-22-3p interacted with the 3' untranslated region segment of NLRP3 (nucleotide-binding domain leucine-rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR-223-3p and miR-22-3p was observed in both mice air pouch synovium and phorbol myristrate acetate-treated THP-1 cells stimulated with monosodium urate (P<.05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR-223-3p and miR-22-3p overexpression group significantly decreased after 6hours of monosodium urate treatment in vivo and in vitro (P<.05). The results of the dual-luciferase reporter assay demonstrated that miR-223-3p and miR-22-3p directly targeted NLRP3. The findings of the present study show that miR-223-3p and miR-22-3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3. The findings of the present study show that miR-223-3p and miR-22-3p can reduce the inflam

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