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


Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Тек жазылушылар үшін

Аннотация

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.

Авторлар туралы

D. Chepurnova

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

Email: erihter@mail.ru
Ресей, Moscow

Е. Samoilova

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

Хат алмасуға жауапты Автор.
Email: erihter@mail.ru
Ресей, Moscow

А. Verin

Vascular Biology Center and Pulmonary Division at Augusta University

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

A. Fesenko

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

Email: erihter@mail.ru
Ресей, Moscow

А. Anisimov

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

Email: erihter@mail.ru
Ресей, Moscow

A. Korotaeva

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

Email: erihter@mail.ru
Ресей, Moscow


© Springer Science+Business Media, LLC, part of Springer Nature, 2019

Осы сайт cookie-файлдарды пайдаланады

Біздің сайтты пайдалануды жалғастыра отырып, сіз сайттың дұрыс жұмыс істеуін қамтамасыз ететін cookie файлдарын өңдеуге келісім бересіз.< / br>< / br>cookie файлдары туралы< / a>