Soluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells

Iranian Journal of Basic Medical Sciences
Chunling MaShichao Xing

Abstract

Hyperuricemia is a risk for cardiovascular and metabolic diseases, but the mechanism is ambiguous. Increased intestinal permeability is correlated with metabolic syndrome risk factors. Intestinal epithelial cells play a pivotal role in maintaining intestinal permeability. Uric acid is directly eliminated into intestinal lumen, however, the mechanism and effect of uric acid on intestinal epithelial cells is poorly explored. Here we carried out an analysis to identify the effect and mechanism of uric acid on intestinal epithelial cells. IEC-6 was exposed to different concentrations of uric acid to simulate the effect of uric acid on intestinal epithelial cells. Cell viability was determined by MTS assay. Protein content and mRNA were assessed using Western blotting and Q-PCR, respectively. Intracellular ROS was determined using flow-cytometry and fluorescence microscopy. Mitochondrial membrane potential was detected by immunofluorescence using a mitochondrial membrane potential assay kit with JC-1. Small interfering RNA transfection was used to suppress the expression of TLR4. We found soluble uric acid alone increased the release of ROS, depolarized the mitochondrial membrane potential, up-regulated TSPO, increased the expressio...Continue Reading

Citations

Oct 20, 2020·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Qiulan LvShichao Xing

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Methods Mentioned

BETA
IECs
polarizing microscopy
Assay
PCR
scraping
electrophoresis
ELISA
flow-cytometry

Software Mentioned

Pro Plus
SDS
Image
SPSS
Primer

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