It is estimated that 90% of hyperuricemia cases are attributed to the inability to excrete uric acid (UA). The two main organs in charge of excreting UA are the kidney (70%) and intestine (30%). Previous studies have reported that punicalagin (PU) could protect against kidney and intestinal damages, which makes it a potential candidate for alleviating hyperuricemia. However, the effects and deeper action mechanisms of PU for managing hyperuricemia are still unknown. To investigate the effect and action mechanisms of PU for ameliorating hyperuricemia. The effects and action mechanisms of PU on hyperuricemia were assessed using a hyperuricemia mice model. Phenotypic parameters, metabolomics analysis, and 16S rRNA sequencing were applied to explore the effect and fundamental action mechanisms inside the kidney and intestine of PU for improving hyperuricemia. PU administration significantly decreased elevated serum uric acid (SUA) levels in hyperuricemia mice, and effectively alleviated the kidney and intestinal damage caused by hyperuricemia. In the kidney, PU down-regulated the expression of UA resorption protein URAT1 and GLUT9, while up-regulating the expression of UA excretion protein ABCG2 and OAT1 as mediated via the activation of MAKP/NF-κB in hyperuricemia mice. Additionally, PU attenuated renal glycometabolism disorder, which contributed to improving kidney dysfunction and inflammation. Similarly, PU increased UA excretion protein expression via inhibiting MAKP/NF-κB activation in the intestine of hyperuricemia mice. Furthermore, PU restored gut microbiota dysbiosis in hyperuricemia mice. This research revealed the ameliorating impacts of PU on hyperuricemia by restoring kidney and intestine damage in hyperuricemia mice, and to be considered for the development of nutraceuticals used as UA-lowering agent.

Fructose and its polysaccharides are widely found in fruits and vegetables, with the Maillard reaction of fructose affecting food quality. This study aimed to investigate the Maillard reaction of fructose using a fructose–histidine model system. The reaction process was characterized using fluorescence spectroscopy and ultraviolet spectroscopy. The effects of temperature, initial reactant concentration, initial fructose concentration, initial histidine concentration, and initial pH value on the different stages of the Maillard reaction were studied. Reactant reduction, ultraviolet and fluorescence spectra, acetic acid content, 5-hydroxymethylfurfural (5-HMF) content, and browning intensity were evaluated. The results showed that increasing the temperature and reactant concentration promoted the condensation reaction of fructose and amino acid in the early stage, the formation of intermediate products with ultraviolet absorption and fluorescence in the intermediate stage, and the formation of pigment in the final stage. The 5-HMF concentration decreased with increasing histidine concentration and initial pH value. Changes in the shape of ultraviolet and fluorescence spectra showed that the initial pH value affected not only the reaction rate, but also the intermediate product types. The 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging rate of the Maillard reaction products increased with increasing temperature, reactant concentration, and initial pH value.