Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury withLarge-Volume Ventilation

摘要

Ventilator-induced lung injury (VILI) is a common complication that results fromtreatment with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS)patients. The present study investigated the effect of endothelial progenitor cell (EPC)transplantation on VILI. Wistar rats were divided into three groups ( =8): sham (S), VILI model (V) induced by tidal volume ventilation (17 mL/kg), and VILI plusEPC transplantation (VE) groups. The lung PaO /FiO ratio, pulmonarywet-to-dry (W/D) weight ratio, number of neutrophils, total protein, neutrophil elastaselevel, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum wereexamined. Furthermore, the histological and apoptotic analysis, and lung tissue proteinexpression analysis of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase (MMP)-9,total nuclear factor kappa B (total-NF-κB), phosphorylated NF-κB (phospho-NF-κB) andmyosin light chain (MLC) were performed. The ventilation-induced decrease inPaO /FiO ratio, and the increase in W/D ratio and total proteinconcentration were prevented by the EPC transplantation. The EPC transplantation (VEgroup) significantly attenuated the VILI-induced increased expression of tumor necrosisfactor (TNF)-α, interleukin (IL)-1β, IL-8, MMP-9, phospho-NF-κB and MLC, neutrophilelastase levels and neutrophil counts in BALF. In addition, the anti-inflammatory factorIL-10 increased in the VE group. Furthermore, pulmonary histological injury and apoptosis(TUNEL-positive cells, increase in Bax and cleaved caspase-3) were considerably diminishedby the EPC transplantation. The EPC transplantation ameliorated the VILI. The mechanismmay be primarily through the improvement of epithelial permeability, inhibition of localand systemic inflammation, and reduction in apoptosis.