Abstract:In this work，high glucose-induced HT-22 cells were employed as a model of insulin neuron damage in the brain to evaluate thiamine′s neuroprotective impact on HT-22 cell damage generated by high glucose.The results showed that thiamine significantly increased intracellular glucose consumption，as evidenced by an increase in fluorescence intensity and glucose uptake concentration of the glucose uptake fluorescent probe 2-[N-（7-nitrobenz-2-oxa-1，3-diazol-4-yl） amino]-2-deoxy-D-glucose （2-NBDG），as well as a significant increase in insulin secretion in HT-22 cells induced by high glucose.Western blot tests showed that thiamine dramatically boosted synapse-related protein expression and regulated β-Catenin/GSK-3β protein expression in cells.The above experimental results showed that thiamine may control intracellular glucose consumption and uptake through the β-Catenin/GSK-3β signaling pathway，thus boosting the expression of synapse-related proteins and reducing high glucose-induced neuron damage.