Fig. 2. Effects of protectin DX on lung tissue ultrastructure and alveolar fluid clearance in LPS-induced acute lung injury in vivo.

Protectin DX (5 µg/kg) was injected into the caudal veins of Sprague-Dawley rats 8 h after LPS (14 mg/kg) stimulation; the rats were then ventilated for 60 min, and the effects of protectin DX were assessed by electron microscope photomicrographs of the lung tissues from rats. The lamellar bodies in the LPS group were severely vacuolated compared with those in the control group; however, the lamellar body damage was recovered in the protectin DX treatment group (a). The control group presented a normal air–blood barrier. In contrast, the air–blood barrier in the LPS group was damaged and had broken epithelial bridges and capillary walls in the tissues. In the treatment group, protectin DX significantly improved the damage to the air–blood barrier induced by LPS (b). lb lamellar body, bc blood capillary, ac air capillary, ep epithelial bridge, en endothelial cell, ecm extracellular matrix of the capillary wall, cn cell nucleus, er erythrocyte. After intratracheal instillation of a 5% albumin solution containing Evans blue-labeled albumin (5 ml/kg) through a tracheostomy to the left lung, alveolar fluid clearance was measured over 60 min in ventilated animals (c). The data are presented as the mean ± SD. n = 8. PDX protectin DX. Alcohol was the solvent for protectin DX. **p < 0.01 versus the control group; ^††p < 0.01 versus the LPS group; ^‡‡p < 0.01 versus the LPS + alcohol group