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[氧自由基在博来霉素诱导的肺纤维化中的作用]

[The role of oxygen radicals in bleomycin-induced pulmonary fibrosis].

作者信息

Wang X Z

机构信息

Respiratory Disease Research Laboratory, Union Hospital, Tongji Medical University Wuhan.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 1992 Jun;15(3):158-60, 191.

PMID:1282089
Abstract

A model of pulmonary fibrosis in rat has been developed using intratracheal administration of bleomycin (BLM) A5 (5mg/kg). Histopathologic features and total lung collagen were studied. We found that type I pneumocytes detached, basement membrane denuded and endothelia edema were the earliest changes in BLM induced pulmonary fibrosis. Serum MDA (an index of lipid peroxidation) level in rats receiving intratracheal bleomycin were increased at earlier time after bleomycin administration. Meanwhile, MDA level in the lung homogenate was elevated too. Our results indicated that the injured type I pneumocytes and endothelia caused by oxygen radicles are the fundamental damages in bleomycin-induced pulmonary fibrosis.

摘要

通过气管内给予博来霉素(BLM)A5(5mg/kg)建立了大鼠肺纤维化模型。研究了组织病理学特征和肺总胶原含量。我们发现,I型肺泡上皮细胞脱离、基底膜剥脱和内皮细胞水肿是博来霉素诱导的肺纤维化最早出现的变化。气管内给予博来霉素的大鼠血清丙二醛(脂质过氧化指标)水平在博来霉素给药后的早期升高。同时,肺匀浆中的丙二醛水平也升高。我们的结果表明,氧自由基导致的I型肺泡上皮细胞和内皮细胞损伤是博来霉素诱导的肺纤维化的根本损伤。

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