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. 2021 Aug 5;2021:1653392. doi: 10.1155/2021/1653392

Table 1.

Inflammatory mechanism of uric acid.

Secretion/expression Cell Mechanism Reference
IL-1 Lymphocyte Activation of inflammasome and caspase-1 complex via P2X7 receptor [17]
IL-1β Macrophage Activate the inflammasome via P2X7 signaling, and treatment with a P2X7 inhibitor reduces IL-1β release [18]
IL-1β Human umbilical vein endothelial cells (HUVECs) Regulate the activation of NLRP3 inflammasome by activation of ROS and K + efflux [19]
IL-6 and TNF-α Human umbilical vein endothelial cells (HUVECs)  High concentrations of UA significantly increased mRNA expression and extracellular release of HMGB1 from human umbilical vein endothelial cells (HUVECs) [23]. Extracellular HMGB1 binding to RAGE activates NF-κB, which leads to proinflammation. [21]
IL-1β Renal tubular epithelial cells (HK-2) UA, like Lipopolysaccharides (LPS), significantly enhanced the expression of TLR4, NLRP3, IL-1β, and ICAM-1 [22]