The effect of vitamin C on the JAK/STAT3 pathway in ischemic stroke: based on the molecular interaction between FOXP3 protein and stat3 protein.

Vitamin C, as an important antioxidant, has been widely studied in recent years for its protective effect in ischemic stroke. FOXP3 protein, as a key transcription factor for regulatory T cell (Treg) function, is closely related to the JAK/STAT3 signaling pathway. This study aimed to investigate the effects of vitamin C on the JAK/STAT3 pathway in ischemic stroke, focusing on the molecular interaction between FOXP3 and STAT3. To uncover its potential therapeutic mechanisms, a transient middle cerebral artery obstruction (MCAO) model was used to evaluate the effect of vitamin C on neurological impairment after ischemic stroke. Behavioral function was assessed by Garcia JH score, protein expression and cell infiltration were detected by Western blotting, flow cytometry and immunofluorescence staining, and peripheral blood mononuclear cells (PBMC) were isolated and analyzed. Statistical methods were used to evaluate the significance of the experimental results. The results showed that vitamin C significantly reduced nerve dysfunction and neuronal cell injury after ischemic stroke, and reduced glial cell infiltration in the injured area. Vitamin C also affected the proportion of regulatory T cells in ischemic stroke and in vitro experiments, and improved ischemic stroke damage by activating the Treg-STAT family, a process closely associated with FOXP3 and STAT3 interactions.