Foodborne prevention and treatment of hyperuricemia (HUA) has received widespread attention. Lactic acid bacteria (LAB) can improve intestinal function, while traditional medicine dandelion has the functions of detoxification and detumescence. Whether LAB fermented dandelion has any effects on HUA and the underlying mechanism is not clear. To address these questions, Lactobacillus acidophilus was selected or maximal xanthine oxidase activity. The effect of Lactobacillus acidophilus fermented dandelion (LAFD) on uric acid metabolism was evaluated by the HUA mouse model. Expression levels of UA, BUN, CRE, XOD, and inflammatory factors in serum were detected. Paraffin sections and staining were used to observe the kidney and small intestine, and mRNA expression of GLUT9, URAT1, OAT1, and ABCG2 related to uric acid metabolism were investigated. Furthermore, the intestinal flora was studied by contents of the cecum and high throughput 16S rRNA sequencing. The results showed that LAFD had a significant inhibitory effect on XOD in vitro (p < 0.01). LAFD could reduce the levels of UA, BUN, CRE, XOD, IL-1 β, IL-6, and TNF- α in serum (p < 0.05), thus inhibiting inflammatory reaction, and reducing UA by decreasing the mRNA expression of GLUT9, URAT1 in kidney and increasing the mRNA expression of OAT1 and ABCG2 in kidney and small intestine (p < 0.05). In addition, the 16S rRNA gene sequencing analysis demonstrated that LAFD treatment can help restore the imbalance of the intestinal microbial ecosystem and reverse the changes in Bacterodietes/Firmicutes, Muribaculaceae, Lachnospiraceae in mice with HUA. It is suggested that the mechanism of LAFD in treating HUA may be related to the regulation of the mRNA expressions of GLUT9, URAT1, OAT1, and ABCG2 in the kidney and small intestine, as well as the regulation of intestinal flora, which provides the experimental basis for the development of new plant fermented products.

Background: To use network pharmacology and gut microbiota sequencing to investigate the probable mechanism of Bining decoction (BN) in the treatment of gouty nephropathy (GN).Methods: Firstly, the mechanism of therapeutic effects of BN on GN were collected by integrating network pharmacology. Secondly, the treatment effects of BN against GN in 30 Institute of Cancer Research (ICR) mice were evaluated by performing biochemical tests [uric acid, blood urea nitrogen, and creatinine (UA, BUN, and Cr)] and evaluating the renal weight index. Finally, 16S rRNA sequencing was utilized for elucidating the therapeutical effect of BN in GN. Results:The results of gut microbiota sequencing analysis showed the abundance of Faecalibaculum,

Hyperuricemia nephropathy, also known as gouty nephropathy, refers to renal damage induced by hyperuricemia caused by excessive production of serum uric acid or low excretion of uric acid. the persistence of symptoms will lead to changes in renal tubular phenotype and accelerate the progress of renal fibrosis. The existence and progressive aggravation of symptoms will bring a heavy burden to patients, their families and society, affect their quality of life and reduce their well-being. With the increase of reports on hyperuricemia nephropathy, the importance of related signal pathways in the pathogenesis of hyperuricemia nephropathy is becoming more and more obvious, but most studies are limited to the upper and lower mediating relationship between 1 or 2 signal pathways. The research on the comprehensiveness of signal pathways and the breadth of crosstalk between signal pathways is limited. By synthesizing the research results of signal pathways related to hyperuricemia nephropathy in recent years, this paper will explore the specific mechanism of hyperuricemia nephropathy, and provide new ideas and methods for the treatment of hyperuricemia nephropathy based on a variety of signal pathway crosstalk and personal prospects.