Polydatin alleviates adenine-induced nephropathy in mice

Adenine-induced nephropathy (AIN) serves as a classic experimental model for studying uric acid-related renal injury, characterized by tubular obstruction, inflammatory cell infiltration, tubular epithelial cell apoptosis, and progressive interstitial fibrosis, among others. These pathological changes are primarily driven by intrarenal deposition of adenine metabolites, and the model reliably recapitulates both hyperuricemia and impaired renal function. The aim of this study was to assess the renoprotective potential of polydatin (PD) in a murine model of AIN.

Fifty male mice (weight, 20 ± 2 g) obtained from The Institute of Cancer Research were randomly assigned into five groups (n = 10 each): normal, AIN model, PD treatment, allopurinol treatment, and desuric benzbromarone (DB) treatment. Changes in oxidative stress, inflammatory response, apoptosis, fibrosis, renal function, and pathological morphology of renal tissue were investigated in mice with AIN.

The outcomes of the present study revealed that renal function and renal histopathology in mice were significantly abnormal in the AIN group. After treatment with PD, it was observed that these abnormal indices were significantly improved, and the structure and function of renal histopathology were significantly protected.

PD exhibited a significant therapeutic effect in mice with AIN, which may play a role in protecting the kidneys by regulating various biological processes such as immune inflammation, apoptosis, and fibrosis, providing an important experimental basis and theoretical basis for the clinical use of PD in treating AIN.