Cytochrome P450 2J3/epoxyeicosatrienoic acids mediate the cardioprotection induced by ischaemic post-conditioning, but not preconditioning, in the rat.

1. Cytochrome P450 (CYP) epoxygenases and their arachidonic acid metabolites play a protective role against ischaemia-reperfusion injury. In the present study, we investigated whether endogenous CYP2J3/epoxyeicosatrienoic acid (EET) mediates the cardioprotective effects of ischaemic preconditioning (IPC) and ischaemic post-conditioning (IPost).

Apelin protects heart against ischemia/reperfusion injury in rat.

Apelin, the endogenous ligand of the G protein-coupled APJ receptor, is a peptide mediator with emerging regulatory actions in the heart. We aimed to determine whether the endogenous apelin/APJ system is an intrinsic protective pathway in ischemic/reperfusion injury. A Langendorff model of perfused isolated rat hearts and primary cultured myocardial cells from neonatal rats were used.

[Effects of 11, 12-epoxyeicosatrienoic acid preconditioning and postconditioning on Ca(2+)- handling proteins in myocardial ischemia/reperfusion injury in rats].

Objective: To investigate the effects of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) preconditioning and postconditioning on Ca(2+)-handling proteins in myocardial ischemia/reperfusion (IR) injury in rats and reveal the effects and mechanism of 11, 12-EET on cardioprotection. METHODS The IR injury model was built by stopping perfusion for 40 minutes followed by reperfusion for 30 minutes. The isolated Langendorff-perfused rat hearts were divided into 4 groups: control group, IR group, EET preconditioning (Pre-EET) group and EET postconditioning (Post-EET) group.

[Effect of 11, 12-epoxyeicosatrienoic acids on hypoxia/reoxygenation injury in the human umbilical vein endothelial cells].

Objective: To investigate the effects of 11, 12-epoxyeicosatrienoic acids (11, 12-EET) on the degree of hypoxia/reoxygenation injury in human umbilical vein endothelial cells ( HUVECs), and reveal the possible pathway of EET on protection.

Methods: Primary cultured HUVECs were randomly divided into control group, hypoxia/reoxygenation group, 11, 12-EET control group, 11, 12- EET hypoxia/reoxygenation group, inhibition of extracellular signal-regulated kinase (ERKI/2) group, and inhibition of nitric oxide synthase (NOS) group. Hypoxia/reoxygenation injury model in HUVECs was established by exposure to hypoxia (2% O2, 5% CO2 and 93% N2) for 3 hours, followed by reoxygenation (95% air and 5% CO2) for 1 hour.