actinonin and Acute-Lung-Injury

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.

Topics: Acute Lung Injury; Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Hydroxamic Acids; Lipopolysaccharides; Lung; Male; Organ Size; Pulmonary Edema; Rats; Rats, Sprague-Dawley; Tiopronin