Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pre-treated ECFCs. After 24 h of CPB, pulmonary capillary permeability, including the PaO2/FiO2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight were evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score 1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74; PaO2/FiO2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30; wet/dry weight 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57; protein levels in BALF: 134 ± 22 vs 442 ± 99 vs 225 ± 41 vs 337 ± 53, all P < 0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO2/FiO2. Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with the CPB/ECFC group, all the indicators were partly reversed by the L-NIO. ECFCs significantly reduced lung injury induced by inflammation after CPB.

中文翻译：

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内皮集落形成细胞减少了大鼠体外循环诱导的肺损伤。

体外循环 (CPB) 通过炎症和内皮损伤导致严重的肺损伤。本研究的目的是评估内皮集落形成细胞 (ECFCs) 对 CPB 大鼠肺损伤的影响。将 32 只大鼠随机分为假手术组、CPB、CPB/ECFC 和 CPB/ECFC/L-NIO 组。假手术组大鼠进行麻醉，其他组大鼠进行体外循环。大鼠还接受了 PBS、ECFC 和 L-NIO 预处理的 ECFC。CPB 24 小时后，评估肺毛细血管通透性，包括 PaO2/FiO2 比值、支气管肺泡灌洗液 (BALF) 中的蛋白质水平和肺组织湿/干重。测试了BALF和外周血中的细胞数和细胞因子。评估内皮损伤、肺组织学损伤和细胞凋亡。分析了氧化应激反应和细胞凋亡相关蛋白。CPB后，与S组获得的数据相比，所有数据均恶化（sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO：组织学评分1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74； PaO2/FiO2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30；湿/干重 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57 ± 2 ± 2 LF 水平 vs 3 ± 4 LF：2 99 对 225 ± 41 对 337 ± 53，所有 P < 0.05）。与 CPB 治疗相比，ECFCs 显着改善了肺毛细血管通透性和 PaO2/FiO2。同样，ECFCs 还减少了 BALF 和外周血中的炎症细胞数量和促炎因子，以及肺组织中的氧化应激反应。ECFCs 降低了肺组织学损伤评分和细胞凋亡，并调节了肺组织中的细胞凋亡相关蛋白。与CPB/ECFC组相比，所有指标均被L-NIO部分逆转。ECFCs 显着减少 CPB 后炎症引起的肺损伤。