Article Summary
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].现代生物医学进展英文版,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
Received:July 30, 2019  Revised:August 25, 2019
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)
Author NameAffiliationE-mail
ZHOU Jia-tian Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, China 863830856@qq.com 
LIANG Wei-dong Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, China  
ZENG Xiao-fei Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, China  
SHANG Guan-sheng Chengdu Seventh People's Hospital, Chengdu, Sichuan, 610500, China  
LIAO Shi-jun Sichuan Fourth People's Hospital, Chengdu, Sichuan, 610500, China  
WU Peng Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, China  
YAN Shen-chao Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, 610500, China  
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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.
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