Further, using a rat model of sepsis and PEVs generated from thrombin-stimulated rat platelets, we demonstrated that PEVs promote NET formation (Histone H3, MPO, HMGB1), endothelial dysfunction (angiopoietin-2 (D), endocan (E) and syndecan-1) and aggravate the inflammatory response (IL-1, IL-6, TNF-α, and MCP-1) in sepsis. This evidence concerns the gene HMGB1 and endothelial dysfunction.