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Vascular inflammation is considered as an important stage in pulmonary artery hypertension.Whether 15-hydroxyeicosatetraenoic acid (15-HETE) plays a role in pulmonary inflammation remains unknown.To investigate this, Western blot, RT-PCR, immunohistochemisty, immunofluorescence and luciferase were performed,and novel evidence showed that hypoxia induced macrophage infiltration, expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were markedly inhibited by NDGA, 15-HETE inhibitor.15-HETE enhanced both adhesion molecules in pulmonary arterial endotheliu1m cells (PAECs) in a time-and concentration-dependent manner.Furthermore, hypoxia promoted 15-Lipoxygenase expression was abolished by NF-κB inhibitors and 15-HETE markedly increased NFκB activity, suggesting a positive feedback mechanism.In conclusion, 15-HETE stimulates ICAM-1 and VCAM-1 in PAECs, which depends mainly on its positive interaction with NF-κB.Thus, a novel mechanism is suggested for hypoxia-induced pulmonary arterial inflammation.