Multi-omics analysis reveals that ginsenoside Rb1 improves prognostic outcomes in sepsis by modulating mitochondrial metabolism MTHFD2 targets.

Sepsis has emerged as a major threat to human mortality. Increasing evidence explores the impact of mitochondrial metabolism on the prognosis of sepsis patients and its therapeutic potential. To enhance risk stratification and identify potential targets, we conducted a retrieval and analysis of differential expression of mitochondrial metabolism related genes (MMRG) between sepsis and normal samples from public databases. Immune infiltration analysis was preformed to gain comprehensive knowledge of features of the established risk model. Additionally, single-cell sequencing results suggested MTHFD2 may be a critical target in sepsis for regulating immune infiltration characteristics, potentially altering platelet metabolism pathways significantly, thereby influencing sepsis occurrence and progression. Utilizing molecular docking, we further screened Ginsenoside Rb1 (Grb1) as a key pharmacological target interacting with MTHFD2. Further animal experiments preliminarily indicated that Grb1 administration was associated with reduced MTHFD2 expression and improved organ function and survival in CLP-induced septic rats. These findings provide new insights and potential therapeutic targets for clinical treatment of sepsis in the future.