Xu Mingjun, Li Xiaoguo, Ma Chen, Lü Yuzhen, Ma Xiaona, Ma Xiaowei
Clinical Medical College of Ningxia Medical University, Yinchuan Ningxia, 750003, P.R.China;Institute for Ningxia Human Stem Cell Research, Yinchuan Ningxia, 750004, P.R.China.
Clinical Medical College of Ningxia Medical University, Yinchuan Ningxia, 750003, P.R.China.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2020 Mar 15;34(3):387-392. doi: 10.7507/1002-1892.201909070.
To investigate the effects of human placental mesenchymal stem cells (hPMSCs) transplantation on pulmonary vascular endothelial permeability and lung injury repair in mice with lipopolysaccharide (LPS)-induced acute lung injury (ALI).
The hPMSCs were isolated from the human placental tissue by enzyme digestion and passaged. The cell phenotype of the 3rd generation hPMSCs was detected by flow cytometry. Twenty-four 6-week-old healthy male C57BL/6 mice were randomly divided into 3 groups ( =8). The mice were instilled with LPS in the airway to prepare an ALI model in the ALI model group and the hPMSCs treatment group, and with saline in the control group. At 12 hours after LPS infusion, the mice were injected with 3rd generation hPMSCs via the tail vein in hPMSCs treatment group and with saline in the ALI model group and the control group. At 24 hours after injection, the lung tissues of all mice were taken. The pathological changes were observed by HE staining. The wet/dry mass ratio (W/D) of lung tissue was measured. The Evans blue leak test was used to detect the pulmonary vascular endothelial permea bility in mice. The expression of lung tissue permeability-related protein (VE-cadherin) was detected by Western blot.
Flow cytometry examination showed that the isolated cells had typical MSCs phenotypic characteristics. Mice in each group survived. The alveolar structure of the ALI model group significantly collapsed, a large number of inflammatory cells infiltrated, and local alveolar hemorrhage occurred; while the alveolar structure collapse of the hPMSCs treatment group significantly improved, inflammatory cells infiltration significantly reduced, and a few red blood cells were in the interstitial lung. W/D and exudation volume of Evans blue stain were significantly higher in the ALI model group than in the control group and the hPMSCs treatment group ( <0.05), in the hPMSCs treatment group than in the control group ( <0.05). The relative protein expression of VE-cadherin was significantly lower in the ALI model group than in the control group and the hPMSCs treatment group ( <0.05), and in the hPMSCs treatment group than in the control group ( <0.05).
Intravenous injection of hPMSCs can effectively reduce the increased pulmonary vascular endothelial permeability mediated by LPS, relieve the degree of lung tissue damage, and play a therapeutic role in ALI mice.
探讨人胎盘间充质干细胞（hPMSCs）移植对脂多糖（LPS）诱导的急性肺损伤（ALI）小鼠肺血管内皮通透性及肺损伤修复的影响。
采用酶消化法从人胎盘组织中分离hPMSCs并传代培养。通过流式细胞术检测第3代hPMSCs的细胞表型。将24只6周龄健康雄性C57BL/6小鼠随机分为3组（每组n = 8）。ALI模型组和hPMSCs治疗组经气道滴注LPS制备ALI模型，对照组滴注生理盐水。LPS注入后12小时，hPMSCs治疗组经尾静脉注射第3代hPMSCs，ALI模型组和对照组注射生理盐水。注射后24小时，取所有小鼠的肺组织。通过HE染色观察病理变化。测量肺组织的湿/干质量比（W/D）。采用伊文思蓝渗漏试验检测小鼠肺血管内皮通透性。通过蛋白质印迹法检测肺组织通透性相关蛋白（VE-钙黏蛋白）的表达。
流式细胞术检测显示，分离的细胞具有典型的间充质干细胞表型特征。各组小鼠均存活。ALI模型组肺泡结构明显塌陷，大量炎性细胞浸润，局部肺泡出血；而hPMSCs治疗组肺泡结构塌陷明显改善，炎性细胞浸润明显减少，肺间质有少量红细胞。ALI模型组的W/D及伊文思蓝染色渗出量显著高于对照组和hPMSCs治疗组（P <0.05），hPMSCs治疗组高于对照组（P <0.05）。ALI模型组VE-钙黏蛋白的相对蛋白表达显著低于对照组和hPMSCs治疗组（P <0.05），hPMSCs治疗组低于对照组（P <0.05）。
静脉注射hPMSCs可有效降低LPS介导的肺血管内皮通透性升高，减轻肺组织损伤程度，对ALI小鼠发挥治疗作用。
