Cytoprotective effect of prostacyclin on hepatic ischemia-reperfusion injury

Table 1 Overproduced molecules and its consequences in hepatic ischemia-reperfusion injury

Number	Molecule	Effect
1	Tumor necrosis factor α	Central mediator with multifactorial effect
2	Interleukin-1α	Mediator of neutrophil infiltration
3	Interleukin-1β	Induction of prostaglandin synthesis, enhancement of T-cell and neutrophil activation and cytokine production
4	Interleukin-12	Induction and development of hepatic ischemia-reperfusion injury
5	Interferon-γ	Increases or reduces neutrophil accumulation in a dose-depend manner
6	Damage-associated molecular patterns	Pro- and anti-inflammatory mediators that promote tissue damage
7	Intercellular adhesion molecule 1	Promotes neutrophil accumulation
8	Vascular cell adhesion molecule 1	Mediates inflammation and promotes neutrophil migration
9	P-selectin	Promotes neutrophil and platelets adhesion
10	Transforming growth factor-β	Promotes vessel wall inflammation and increase vascular permeability
11	Vascular endothelial growth factor	Promotes T lymphocyte, macrophage and neutrophil accumulation
12	Plasminogen activator inhibitor 1	Promotes neutrophil accumulation and suppresses fibrinolysis
13	Nitric oxide	Prevents or promotes cell damage depending on NO synthesis processes
14	Endothelin-1	Vasoconstriction
15	Combination of released factors	Heart-kidney damage, systematic inflammatory response syndrome SIRS, multiple organ dysfunction, death