Fig. 1

Proposed pathophysiological mechanisms involved in SAE. SAE Sepsis-associated encephalopathy, TNF-α tumour necrosis factor alpha, IL-1β Interleukin 1beta, HMGB1 High-mobility group box 1, VCAM-1 Vascular cell adhesion molecule 1, ICAM-1: Intercellular adhesion molecule 1, SOD Superoxide dismutase, CAT Catalase, NO Nitric oxide, ROS Reactive oxygen species, RNS Reactive nitrogen species, PMN Polymorphonuclear cells, mtROS mitochondrial reactive oxygen species, GPX Glutathione peroxidase, MDA Malondialdehyde, MPO Myeloperoxidase, MMP Mitochondrial membrane potential, DCA Dynamic cerebral autoregulation, NVC Neurovascular coupling, CBF Cerebral blood flow, ZO-1 Zonular occludens 1, CC3 Cleaved caspase 3, Tregs Regulatory T cells, Th2 helper T cells