Human fetal membrane IL-1β production in response to bacterial components is mediated by uric-acid induced NLRP3 inflammasome activation

2021 ◽  
pp. 103457
Author(s):  
Alex S. Miller ◽  
Tiffany N. Hidalgo ◽  
Vikki M. Abrahams
Keyword(s):  
Uric Acid ◽  
Nlrp3 Inflammasome ◽  
Fetal Membrane ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals Methyl Gallate Improves Hyperuricemia Nephropathy Mice Through Inhibiting NLRP3 Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Peng Liu ◽  
Wen Wang ◽  
Qiang Li ◽  
Xin Hu ◽  
Bingyong Xu ◽  
...  
Keyword(s):  
Uric Acid ◽  
Nlrp3 Inflammasome ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Human Peripheral Blood ◽  
Collecting Duct ◽  
Potassium Oxide ◽  
Inflammasome Activation ◽  
Methyl Gallate ◽  
Nlrp3 Inflammasome Activation

Hyperuricemia nephropathy (HN) is a form of chronic tubulointerstitial inflammation, caused by the deposition of monosodium urate crystals (MSU) in the distal collecting duct and medullary interstitium, associated with a secondary inflammatory reaction. Numerous published reports indicated that NLRP3 inflammasome pathway play crucial roles in HN symptoms. The present study aims to investigate the protective effects of methyl gallate on HN mice and the underlying mechanisms. An HN model was established by intraperitoneal injection of potassium oxide (PO) to assess the effect of methyl gallate on renal histopathological changes, renal function, cytokine levels and expressions of NLRP3-related protein in HN mice. Moreover, in vitro models of lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs) and human peripheral blood mononuclear cells (PBMCs) were established to explore the mechanism of methyl gallate on NLRP3 inflammasome activation. The results showed that methyl gallate significantly ameliorated HN by inhibiting uric acid production and promoting uric acid excretion as well as ameliorating renal injury induced by NLRP3 activation. Mechanistically, methyl gallate is a direct NLRP3 inhibitor that inhibits NLRP3 inflammasome activation but has no effect on the activation of AIM2 or NLRC4 inflammasomes in macrophages. Furthermore, methyl gallate inhibited the assembly of NLRP3 inflammasomes by blocking the ROS over-generation and oligomerization of NLRP3. Methyl gallate was also active ex vivo against ATP-treated PBMCs and synovial fluid mononuclear cells from patients with gout. In conclusion, methyl gallate has a nephroprotective effect against PO-induced HN through blocking the oligomerization of NLRP3 and then exerting anti-inflammatory activity in the NLRP3-driven diseases.

LncRNA ANRIL promotes NLRP3 inflammasome activation in uric acid nephropathy through miR-122-5p/BRCC3 axis

Biochimie ◽  
2019 ◽  
Vol 157 ◽  
pp. 102-110 ◽  
Author(s):  
Jiacai Hu ◽  
Hao Wu ◽  
Daochun Wang ◽  
Zhijie Yang ◽  
Junjun Dong
Keyword(s):  
Uric Acid ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Uric Acid Nephropathy
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