To investigate the effect of polydatin on glucose transporter, blood glucose homeostasis and renal injury in streptozotocin (STZ)-induced diabetic rats. The in vitro inhibitory effect of polydatin on sodium-glucose cotransporter-1 (SGLT1) and 2 (SGLT2) was determined using HEK293 cells. The inhibitory effect of polydatin on GLUT1 and GLUT4 was evaluated using 3T3-L1 adipocytes. Streptozotocin-induced diabetic rats were used for this study. Fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), urea nitrogen, serum creatinine and urinary protein were determined using biochemical analyzer. Histopathological examination was performed on renal tissue. Serum levels of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein 1 (MCP-1) and C-reactive protein (CRP) were also determined. Polydatin significantly inhibited SGLT1/2 and exhibited high selectivity for both GLUT1 and GLUT4. It significantly and dose-dependently decreased hyperglycemia, enhanced urine glucose excretion in the diabetic rats. The polydatin treatment significantly ameliorated symptoms of DN such as polyuria, polydipsia and hyperphagia. The hypoglycemic effect of polydatin was maintained throughout the treatment period. In addition,the levels of IL-1β, TNF-α, MCP-1 and CRP were significantly reduced in treated group. Treatment with polydatin significantly ameliorated most of the structural and morphological changes induced by STZ. Moreover, the levels of urinary protein, serum creatinine and urea nitrogen were significantly reduced after treatment with polydatin. As a potential dual inhibitor of SGLT1/2, polydatin has high selectivity for GLUT1 and GLUT4. Its long-term administration delays the development of DN, protects renal function and ameliorates renal tissue injury.
This study investigated the antiepileptic effects of polydatin (PD) and its potential mechanisms. Racine scoring and EEG were used to assess seizure severity in a PTZ-induced mouse epilepsy model. The results demonstrated that PD significantly reduced the intensity of seizures. Behavioral tests revealed that PD improved learning, memory, and motor coordination. Histological analysis using HE and Nissl staining showed that PD alleviated hippocampal neuronal damage. TUNEL staining further confirmed that PD effectively prevented neuronal apoptosis. Network pharmacology predicted SIRT1 as a potential target of PD, and GO and KEGG pathway enrichment analyses indicated that PD regulated mitochondrial function. Therefore, PD may reduce neuronal damage by protecting mitochondrial function through SIRT1. This process was tested both in vitro and in vivo . In a Mg 2+ -free neuronal excitability model, CCK-8, LDH, and Hoechst staining results demonstrated that PD significantly increased cell survival and reduced apoptosis. Reduced mitosox staining, along with increased activity of Complexes IV and V and ATP production, indicated that PD mitigated mitochondrial function. Gene expression studies revealed that PD activated the SIRT1-PGC-1α signaling pathway via AMPK. In conclusion, PD exerted neuroprotective effects by regulating mitochondrial function, suggesting a potential therapeutic target for epilepsy.
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