Caspase-1 is hepatoprotective during trauma and hemorrhagic shock by reducing liver injury and inflammation.

摘要: Adaptive immune responses are induced in liver after major stresses such as hemorrhagic shock (HS) and trauma. There is emerging evidence that the inflammasome, multiprotein platform induces caspase-1 activation promotes interleukin (IL)-1β IL-18 processing, activated response to cellular oxidative stress, hypoxia, ischemia HS. Additionally, damage-associated molecular patterns, those released injury, have been shown activate inflammasome through NOD-like receptor (NLR) NLRP3. However, role of organ injury HS trauma unknown. We therefore investigated inflammatory end-organ wild-type (WT) caspase-1−/− mice our model with bilateral femur fracture (HS/BFF). found had higher levels systemic cytokines than WT mice. This result corresponded damage, cell death neutrophil influx compared WT, although there was no difference lung damage between experimental groups. To determine if hepatoprotection also depended on NLRP3, we subjected NLRP3−/− HS/BFF, but these similar WT. Hepatoprotection not due caspase-1-dependent cytokines, IL-1β IL-18. Altogether, data suggest hepatoprotective, part regulation pathways trauma, HS/BFF does depend These findings may implications for treatment patients lead progress prevention or multiple failure (MOF).