Mechanism of targeted uric acid reduction by soybean protein peptide SHECN in hyperuricemia mice and improvement of liver injury

Hyperuricemia (HUA) is a chronic condition characterized by abnormal purine metabolism. SHECN (Ser-His-Glus-Cys-Asn), a soy-derived peptide, has demonstrated uric acid (UA) lowering and antioxidant properties in vitro. The aim of this study was to further explore its uric acid lowering potential in hyperuricemia mice. The results indicated that UA level in SHECN-H group (40 mg/kg) was reduced to 32.80±1.23 μmol/L compared with that in HUA group (104.46±7.30 μmol/L). SHECN group decreased serum xanthine oxidase (XO) and adenosine deaminase (ADA) activities, AST and ALT activities. Additionally, SHECN significantly ameliorated fiber damage observed in mouse liver tissue. We also found that under the action of SHECN, the active expression of XO and ADA in serum and liver was down-regulated, and the expression of hypoxanthine-guanine phosphoribosyl transferase (HGPRT) was up-regulated. Notably, SHECN effectively mimics interactions with XO-associated target proteins as well as key liver transporter receptor proteins. This study further confirmed that SHECN can affect the activity level of the key receptor protein of uric acid synthesis in the liver of mice, and ultimately reduce the serum uric acid level and alleviate liver injury ( P < 0.05 ).