作者: Annie Pardo , Roberto Barrios , Vilma Maldonado , Jorge Meléndez , Julia Pérez
DOI: 10.1016/S0002-9440(10)65625-8
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摘要: Subacute hyperoxia may cause basement membrane disruption and subsequent fibrosis. To test the role of extracellular matrix degradation in hyperoxic damage, we analyzed expression gelatinases A B tissue inhibitors metalloproteinases (TIMP)-1 TIMP-2 rats exposed to 85% O 2 . Oxygen-exposed were studied at 1, 3, 5, 7 days, compared with air-breathing rats. Lung mRNAs assayed by Northern situ hybridization showed an up-regulation lung from 3rd day on. Gelatinase was localized alveolar macrophages interstitial epithelial cells. mRNA protein bronchiolar Increased gelatinase activities demonstrated bronchoalveolar lavage. TIMP-1 constitutively expressed, only displayed a moderate increase hyperoxia. elucidate transcriptional mechanisms for increased after hyperoxia, nuclear transcription factor-κβ activation explored. Oxidative stress significantly (p65) protein, levels found isolated type II cells obtained Conceivably, subacute induces excessive activity, which contribute damage.