Dexmedetomidine exerts a neuroprotective effect by inhibiting Th1 cells and actuating Tregs in postoperative inflammation: Molecular structure and mechanism of action of STAT1 protein.

Dexmedetomidine, an α2-adrenergic receptor agonist, has received attention in recent years for its role in reducing perioperative inflammatory response and neuroprotection. The aim of this study was to investigate how dexmedetomidine exerts neuroprotective effects by inhibiting Th1 cells and activating regulatory T cells (Tregs), and to analyze the molecular structure of STAT1 protein and its mechanism in this process. The number and function of Th1 cells and Tregs in peripheral blood and spleen were analyzed following treatment with dexmedetomidine. Additionally, the expression and activation of STAT1 were examined using western blot and immunofluorescence staining. Relevant cytokine levels were quantified in tandem with flow cytometry to evaluate alterations in immune response. The study revealed that dexmedetomidine significantly suppressed the activation of Th1 cells and enhanced the proliferation and function of Tregs. The activation of STAT1 played a crucial regulatory role in the effects of dexmedetomidine, with its expression level exhibiting a negative correlation with Th1 cell activation and a positive correlation with Treg activity. The phosphorylated state of STAT1 changes after treatment with dexmedetomidine, further supporting its key role in immune regulation.