Endothelial nitric oxide synthase and heme oxygenase-1 act independently in liver ischemic preconditioning.

摘要: Abstract Background ischemic preconditioning (IPC) protects against liver ischemia–reperfusion (IR) injury. The mechanism involves nitric oxide metabolism but the importance of endothelial synthase (eNOS) has not been established. Heme oxygenase-1 (HO-1) IR it is unclear if this depends on synthase. Materials and methods A mouse model IPC with using wild-type (WT) eNOS transgenic knockout (eNOS−/−) mice was developed to study role its relationship HO-1. Serum alanine aminotransferase level, histopathologic injury scores, microcirculatory blood flow were measured. Western blots measured HO-1/2, eNOS, phosphorylated inducible synthase, reverse transcription–polymerase chain reaction (HO-1). set 24-h recovery experiments undertaken WT measurement serum histologic score, HO-1 by blot. Results In animals, preceding resulted in a reduction hepatocellular injury, improvement parenchymal perfusion. contrast, eNOS−/− did protect animals from There no difference between expression all groups. protein detected nonrecovery groups messenger RNA experiments, protective IPC + IR only sham group. Conclusions This used an demonstrate that mediates protection IPC. activity are increased independently IR, later stages IR.