Inhibition of Meprins Reduces Pulmonary Edema in LPS-Induced Acute Lung Damage


如何引用文章

全文:

开放存取 开放存取
受限制的访问 ##reader.subscriptionAccessGranted##
受限制的访问 订阅存取

详细

Pulmonary edema is the major factor of tissue hypoxia in acute lung injury. Disruption of cell—cell contacts and lung interstitium increases permeability of the vascular endothelium and alveolar epithelium, which leads to the development of pulmonary edema. Meprin metalloproteases cleave extracellular matrix proteins, thus aggravating pulmonary edema. Meprin inhibitor actinonin was administered to rats with LPS-induced acute lung injury. Damaged lungs looked spotted and had multiple hemorrhage focuses, protein concentration in lavage fluid was increased, and lung weight coefficient was high. Administration of meprin inhibitor actinonin considerably reduced protein content in the bronchoalvelolar lavage and lung coefficient; only solitary lung hemorrhages were seen after this treatment. Thus, inhibition of meprins potentially alleviates LPS-induced disorders in the lung tissue permeability and reduces pulmonary edema.

作者简介

D. Chepurnova

National Medical Research Center for Cardiology, Ministry of Health of the Russian Federation

Email: erihter@mail.ru
俄罗斯联邦, Moscow

Е. Samoilova

National Medical Research Center for Cardiology, Ministry of Health of the Russian Federation

编辑信件的主要联系方式.
Email: erihter@mail.ru
俄罗斯联邦, Moscow

А. Verin

Vascular Biology Center and Pulmonary Division at Augusta University

Email: erihter@mail.ru
美国, Augusta, GA

A. Fesenko

National Medical Research Center for Cardiology, Ministry of Health of the Russian Federation

Email: erihter@mail.ru
俄罗斯联邦, Moscow

А. Anisimov

National Medical Research Center for Cardiology, Ministry of Health of the Russian Federation

Email: erihter@mail.ru
俄罗斯联邦, Moscow

A. Korotaeva

National Medical Research Center for Cardiology, Ministry of Health of the Russian Federation

Email: erihter@mail.ru
俄罗斯联邦, Moscow


版权所有 © Springer Science+Business Media, LLC, part of Springer Nature, 2019
##common.cookie##