Integrated transcriptomic and proteomic profiling reveals C3-associated hippocampal neuroimmune remodeling in sodium bicarbonate-treated sepsis-associated encephalopathy

Background

Sepsis-associated encephalopathy (SAE) is a neurological complication of sepsis characterized by cognitive impairment and persistent brain dysfunction. Although neuroinflammation and glial activation contribute to SAE pathogenesis, the molecular alterations underlying hippocampal neuroimmune dysfunction remain incompletely understood. The potential role of NaHCO₃ in SAE-associated neurological dysfunction remains unclear.