Quercetin Prevents Hyperuricemia Associated With Gouty Arthritis by Inactivating the <scp>NLRP3</scp>/<scp>NF</scp>‐<scp>κB</scp> Signaling Pathway
Qingliang Meng, Chenyang Song, Junfu Ma, Jiakang Cui, Junping Zhan, Jing Zhao, Yunan Zhang, Ze‐Lin Zhu, Xinping Du
Abstract
Quercetin (QCT) shows great therapeutic potential for hyperuricemia (HUA) associated with gouty arthritis (GA). However, the underlying mechanism of QCT in inhibiting the progression of HUA and GA remains unclear. HUA mouse model was established by injection of oteracil potassium (OXO) combined with ethambutol (EMB). The GA mouse model was established by intraarticular injection of sodium urate (MSU). MSU-induced HK-2 cells as well as lipopolysaccharide (LPS) and MSU-induced THP-1/M0 macrophages were used as cell models. The ankle perimeter of each mouse was measured to evaluate ankle swelling. The study also detected serum levels of uric acid (UA), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β (IL-1β), and IL-6 and analyzed the pathological conditions of synovial tissues and renal tissues. QCT treatment inhibited ankle joint swelling, TNF-α, IL-1β, and IL-6 serum levels as well as UA production in HUA and GA mice. Treatment with QCT inhibited oxidative stress in the renal tissues of HUA and GA mice and MSU-induced HK-2 cells. QCT treatment inhibited the inflammatory response in LPS and MSU-induced THP-1/M0 macrophages. QCT treatment inactivated the NOD-like receptor thermal protein domain associated protein 3 (NLRP3)/nuclear factor kappa-B (NF-κB) pathway. QCT inactivated the NLRP3/NF-κB signaling pathway to prevent HUA associated with GA.