中文摘要：

目的观察人胎盘间充质干细胞对小鼠肺纤维化的影响,并探讨其作用机制。方法采用组织块贴壁法分离并体外培养人胎盘间充质干细胞。将30只C57BL/6小鼠随机均分为观察组、对照组,均给予气管内注入博来霉素8.5 mg/kg建立肺纤维化模型。造模成功后,观察组尾静脉输注体外培养的人胎盘间充质干细胞0.3 m L（细胞数为1.0×106个）,对照组注射等量生理盐水,1次/d,连续注射3天;处死小鼠,取肺组织,检测肺组织羟脯氨酸含量,采用Western blotting法检测肺组织血管内皮生长因子（VEGF）、内皮素1（ET-1）和血管生成素2（Ang-2）蛋白。结果观察组肺组织羟脯氨酸含量为（5.76±0.13）μg/m L,对照组为（8.13±0.87）μg/m L,两组比较P〈0.01。观察组肺组织VEGF的相对表达量为52.7±4.7、ET-1为68.1±5.4、Ang-2为59.6±2.8,均较对照组（100）降低（P均〈0.05）。结论人胎盘间充质干细胞可抑制小鼠肺组织纤维化形成;降低肺组织VEGF、ET-1和Ang-2表达可能是其作用机制。

英文摘要：

Objective To observe the effect of placenta-derived mesenchymal stem cells on the pulmonary fibrosis in mice and to explore its mechanism. Methods Human placenta-derived mesenchymal stem cells were isolated and cultured in vitro by tissue explants adherent method. Thirty C57 BL /6 mice were randomly divided into the observation group and the control group,and all mice were injected with 8. 5 mg / kg to establish the model of pulmonary fibrosis. After the models were successful established,mice in the observation group received intravenous injection of placenta-derived mesenchymal stem cells 0. 3 m L（ cell number of 1. 0 × 106）,and mice in the control group were injected with the same amount of normal saline,once a day for 3 days. Then,the mice were killed to collect the lung tissues to determine the content of hydroxyproline. The expression of vascular endothelial growth factor（ VEGF）,endothelin 1（ ET-1） and angiogenin 2（ Ang-2） proteins was determined by Western blotting. Results The hydroxyproline contents in the lung tissue of observation group and control group were respectively（ 5. 76 ± 0. 13） μ / m L and（ 8. 13 ± 0. 87） μg / m L,and significant difference was found between the two groups（ P〈0. 01）. The expression of VEGF,ET-1 and Ang-2 in the lung tissues of the observation group was respectively 52. 7 ± 4. 7,68. 1 ± 5. 4 and 59. 6 ± 2. 8,which was all lower than that of the control group（ all P〈0. 05）. Conclusion Placenta-derived mesenchymal stem cells can inhibit the formation of pulmonary fibrosis and its mechanism may be related with the decreased expression of VEGF,ET-1 and Ang-2 protein in lung tissue.