Mesenchymal stem cells (MSCs) can alleviate acute respiratory distress syndrome (ARDS), but the mechanisms involved are unclear, especially about their specific effects on cellular mitochondrial respiratory function. Thirty mice were allocated into the Control, LPS, and LPS + Bone marrow mesenchymal stem cell (BMSC) group (n = 10/group). Mouse alveolar epithelial cells (MLE-12) and macrophage cells (RAW264.7) were divided into the same groups. Pathological variation, inflammation-related factors, reactive oxygen species (ROS), ATP levels, and oxygen consumption rate (OCR) were analyzed. Pathologic features of ARDS were observed in the LPS group and were significantly alleviated by BMSCs. The trend in inflammation-related factors among the three groups was the LPS group > LPS + BMSC group > Control group. In the MLE-12 co-culture system, IL-6 was increased in the LPS group but not significantly reduced in the LPS + BMSC group. In the RAW264.7 co-culture system, IL-1β, TNF-α, and IL-10 levels were all increased in the LPS group, IL-1β and TNF-α levels were reduced by BMSCs, while IL-10 level kept increasing. ROS and ATP levels were increased and decreased respectively in both MLE-12 and RAW264.7 cells in the LPS groups but reversed by BMSCs. Basal OCR, ATP-linked OCR, and maximal OCR were lower in the LPS groups. Impaired basal OCR and ATP-linked OCR in MLE-12 cells were partially restored by BMSCs, while impaired basal OCR and maximal OCR in RAW264.7 cells were restored by BMSCs. BMSCs improved the mitochondrial respiration dysfunction of macrophages and alveolar epithelial cells induced by LPS, alleviated lung tissue injury, and inflammatory response in a mouse model of ARDS.

中文翻译：

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骨髓干细胞对线粒体功能的影响及缓解ARDS的研究。

间充质干细胞（MSC）可以缓解急性呼吸窘迫综合征（ARDS），但其机制尚不清楚，特别是它们对细胞线粒体呼吸功能的具体影响。30 只小鼠被分配到对照组、LPS 和 LPS + 骨髓间充质干细胞 (BMSC) 组（n = 10/组）。小鼠肺泡上皮细胞（MLE-12）和巨噬细胞（RAW264.7）被分为同一组。分析病理变化、炎症相关因素、活性氧（ROS）、ATP水平和耗氧率（OCR）。LPS组观察到ARDS的病理特征，并且BMSCs显着减轻了ARDS的病理特征。三组间炎症相关因子变化趋势为LPS组>LPS+BMSC组>对照组。在MLE-12共培养体系中，LPS组中IL-6增加，但LPS+BMSC组中IL-6没有显着减少。在RAW264.7共培养体系中，LPS组IL-1β、TNF-α和IL-10水平均升高，BMSCs降低IL-1β和TNF-α水平，而IL-10水平保持不变。增加。LPS组的MLE-12和RAW264.7细胞中ROS和ATP水平分别升高和降低，但被BMSC逆转。LPS 组的基础 OCR、ATP 相关 OCR 和最大 OCR 较低。MLE-12 细胞中受损的基础 OCR 和 ATP 相关 OCR 可以被 BMSC 部分恢复，而 RAW264.7 细胞中受损的基础 OCR 和最大 OCR 可以被 BMSC 恢复。BMSC 改善了 LPS 诱导的巨噬细胞和肺泡上皮细胞的线粒体呼吸功能障碍，减轻了 ARDS 小鼠模型中的肺组织损伤和炎症反应。