ICR mice Targeted loci. ICR mice

This study provides molecular mechanisms by which EH-TDM relief of hyperuricemia, including reducing uric acid formation and promoting uric acid excretion. In the process of purine metabolism, due to lack of the transcription of genes HPRT, purine is degraded to uric acid. EH-TDM can increase the transcription of genes HPRT, so that purine returns to the purine state before being degraded into uric acid, inhibiting the synthesis of uric acid. At the same time, EH-TDM increased the transcription of genes ABCG2, ADRB3, UMOD, decreased the transcription of genes GLUT9, GCKR, promoted the excretion of uric acid, reduces the concentration of serum uric acid in mice, and alleviated the inflammatory reaction caused by excessive uric acid. At the same time, EH-TDM treatment also altered the structure of the gut microbiota in hyperuricemia mice. Therefore, the EH-TDM may help identify alternative strategies for alleviating the effects of hyperuricemia and its safety is evaluated from the perspective of transcription and flora, which provides a theoretical basis for the development of new strategies.