Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions.

摘要: Background: Urinary Trypsin Inhibitor (UTI) is involved in various aspects of tissue repair, regeneration and development. However, the potential role UTI protection against acute lung injury (ALI) remains largely unknown. In present study, we demonstrated that treatment could ameliorate ALI induced by oleic acid (OA) rabbit model. Methods: Intravenous application (10000 U/kg/d) significantly improved pathologies associated with OA-induced ALI. The lungs were stained hematoxylin eosin to scored injury. Peripheral blood mononuclear cells isolated density gradient centrifugation Ficoll-Plaque Plus. proliferation ability tube structure formation EPCs observed level phosphorylated Akt protein expression eNOS assayed. Results: Consistent pathological scores, reduced wet/dry ratio OA injured lungs. A quantification capillary revealed led about 2 fold increase over uninjured control 1.5 PBS treatment. capacity for on ECM gel was group recovered Quantification western blot bands summarized showed activates Akt/eNOS signaling. NO production contribute improvement function Conclusions: UTI-induced phosphorylation/activation Akt, increases intracellular NO, thereby improving EPCs. crucial re-endothelialization after denuding injuries arteries.