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Inhibition by erythromycin of human pulmonary artery endothelial cell injury induced by human neutrophils.

作者信息

Mitsuyama T, Furuno T, Hidaka K, Tanaka T, Abe M, Hara N

机构信息

Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Respiration. 1997;64(3):206-10. doi: 10.1159/000196672.

DOI:10.1159/000196672
PMID:9154672
Abstract

Neutrophils are thought to play a key role in tissue injury. We investigated the role of human neutrophils in the induction of injury to the human pulmonary artery endothelial cells and the effect of erythromycin on neutrophil-induced endothelial cell damage. Incubation of unstimulated neutrophils with endothelial cells increased the release of lactate dehydrogenase (LDH) activity and preloaded fura-2 from endothelial cells. When neutrophils were activated by phorbol myristate acetate, the release of LDH and fura-2 was enhanced further. Superoxide dismutase partially inhibited the release of LDH and fura-2 induced by neutrophils, whereas erythromycin markedly inhibited the release of endothelial cell LDH and fura-2 induced by neutrophils. These results suggest that endothelial cell injury is, at least in part, mediated by the action of superoxide and that erythromycin protects against neutrophil-induced endothelial cell injury.

摘要

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