| 周家田,梁卫东,曾小飞,尚观胜,廖世均,吴 鹏,颜神超.MT2A对脂多糖介导的人肺毛细血管内皮细胞损伤的保护作用[J].,2020,(6):1051-1056 |
| MT2A对脂多糖介导的人肺毛细血管内皮细胞损伤的保护作用 |
| Protective Effect of MT2A on Lipopolysaccharide-mediated Injury of Human Pulmonary Capillary Endothelial Cells |
| 投稿时间：2019-07-30 修订日期：2019-08-25 |
| DOI：10.13241/j.cnki.pmb.2020.06.011 |
| 中文关键词: 金属硫蛋白2A 肺损伤 肺保护 炎性因子 细胞骨架 脂多糖 |
| 英文关键词: Metallothionein 2A Lung injury Lung protection Inflammatory factor Cytoskeleton Lipopolysaccharid |
| 基金项目:四川省教育厅科研重点项目（17ZA0136） |
|
| 摘要点击次数: 960 |
| 全文下载次数: 478 |
| 中文摘要: |
| 摘要 目的：探索不同浓度的金属硫蛋2A(Metallothionein 2A, MT2A)对脂多糖(Lipopolysaccharid, LPS)介导的人肺微血管内皮细胞损伤的保护作用。方法：培养人肺毛细血管内皮细胞株（Human lung microvascular endothelial cells, HPMVECs），经过一定浓度LPS溶液进行刺激后，利用不同浓度的MT2A与对照组共同培养，一段时间后观察炎性介质IL-6、TNF-α释放的量及荧光显微镜观察组HPMVECs骨架形态变化。结果：各组TNF-α浓度均在0 h 最低，随之逐渐升高，到6 h达到高峰；从各时间点来看，除0 h各组TNF-α浓度无显著差异外（F=0.717, P=0.549），其余各时间点B1、B2、B3均显著高于A组（均P<0.05）。各组中IL-6浓度均在0 h 最低，A组在2 h达到高峰，随后逐渐下降；B1组在4 h达到高峰，随之下降；B2、B3组从0 h开始逐渐升高，到6 h达到峰值；从各时间点来看，除0 h各处理因素无显著差异外（F=2.341, P=0.092），其余各时间点B1、B2、B3均低于A组（均P<0.05）。A组6 h小时后纤维状肌动蛋白（F-actin）明显解聚，分布明显减少，应力纤维排列紊乱或者消失；B1组、B2组、B3组6 h小时后，与A组相比，F-actin的分布明显较多，应力纤维排列较为整齐。结论：LPS刺激人肺毛细血管内皮细胞有明显损伤效应，加入MT2A后细胞相关炎性因子释放量、细胞骨架损伤情况明显减轻，表明一定浓度的MT2A对LPS介导的肺毛细血管损伤有明显保护作用。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the protective effects of different concentrations of metallothionein 2A on human lung microvascular endothelial cell injury. Methods: Culture human lung capillary endothelial cell line, stimulated with a certain concentration of LPS solution, and then use different concentrations of MT2A. Co- Cultivation with the control group, the amount of IL-6 and TNF-α released from the inflammatory medium and the morphology of the HPMVECs in the fluorescence microscope group were observed after a period of time. Results: The concentration of TNF-α in each group was the lowest at 0 h, then gradually increased, and reached a peak at 6 h. From the time points, except for 0h, there was no significant difference in the concentration of TNF-α between the groups (F=0.717, P=0.549). At other time points, B1, B2, and B3 were significantly higher than those in group A (both P<0.05). The IL-6 concentration of each group was the lowest at 0 h, and the peak of group A peaked at 2 h, then gradually decreased. The peak of group B1 peaked at 4 h and then decreased. Groups B2 and B3 gradually increased from 0h and peaked at 6 h. From each time point, there was no significant difference (F=2.341, P=0.092) except for 0h treatment factor. B1, B2 and B3 were lower than group A at other time points (all P<0.05). After 6 hours in group A, fibrillating actin (F-actin) depolymerized, the distribution was significantly reduced, and the stress fibers were disordered or disappeared. After 6 hours in the B1, B2 and B3 groups, the distribution of F-actin was significantly more than that of the A group, and the stress fibers were arranged neatly. Conclusion: LPS stimulates human lung capillary endothelial cells to have obvious damage. After the addition of MT2A, the release of cell-associated inflammatory factors and cytoskeletal damage were significantly reduced, indicating that certain concentrations of MT2A have significant protective effects against LPS-mediated pulmonary capillary damage. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
