Mechanism of dihydromyricetin on podocytes in db/db mice based on network pharmacology and molecular docking techniques

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This study explored the therapeutic potential of dihydromyricetin (DHM) on podocytes in diabetic nephropathy (DN) mice using a comprehensive experimental approach. A controlled animal trial was conducted with three groups: normal group (5 db / m mice), model group (5 db / db mice), and DHM group (5 db / db mice). Over an 8-week intervention period, the normal and model groups received saline, while the DHM group received 200 mg/kg DHM every other day. Renal function was assessed via blood glucose, urine protein, creatinine, and blood urea nitrogen (bUN) levels. Renal morphology was assessed using histochemistry and electron microscopy. Network pharmacology was employed to identify DHM targets in DN, with intersecting pathways validated in cellular and animal models. Experimental results demonstrated that after 8 weeks of DHM treatment, the DHM group exhibited reductions in body weight, blood glucose, creatinine, BUN, and urinary protein-to-creatinine ratio, along with improved kidney structures, compared to the model group. Network pharmacology revealed 34 DHM-DN intersection targets, focusing on tumor necrosis factor (TNF), interleukin-6, interleukin-1β, caspase-3, caspase-9, and pathways such as TNF signaling and apoptosis. DHM significantly reduced inflammatory factors and apoptosis in both murine and cellular models. In conclusion, DHM mitigates renal injury in DN by reducing blood glucose, curbing inflammation, and decreasing podocyte apoptosis.