Fig. 2.

Cytokine release in inflammation is mediated by DAMPS binding to TLR4/RAGE receptors on the cell membrane. Both pathways activate NF-κB and NLRP3 inflammasome production, resulting in secretion of pro-inflammatory cytokines [75, 150]. RAGE results in further production of HMGB1 [151]. NLRP3 inflammasome activation results in caspase mediated cell death [119]. Several studies haves demonstrated that RIC modulates NF-κB activity via in both ischaemia and endotoxaemia [74, 76, 92, 117, 130]. TLR4 Toll-like receptor 4, DAMPS damage associated molecular patterns, HMGB1 high mobility group box 1, TNF-α tumour necrosis factor alpha, LPS lipopolysaccharide, RAGE Receptor for advanced glycation end-products, ERK extracellular signal related kinase, MAPK mitogen activated protein kinase, EGR-1 early growth response 1, TAK1 transforming factor-β-activated kinase 1, Iκβ inhibitor kappa beta kinase, NF-κβ nuclear factor kappa beta