摘要
目的探讨烟曲霉对肺微血管内皮细胞通透性的影响及其机制。方法利用激光共聚焦扫描显微镜检测人肺微血管内皮细胞肌动蛋白(F-actin)和细胞跨膜电阻仪测定细胞跨膜电位,以观察细胞通透性的改变,并利用p38 MAPK抑制剂、ROCK抑制剂和蛋白激酶C抑制剂探讨其机制。结果烟曲霉处理后肺微血管内皮细胞Factin染色的荧光强度显著下降(P<0.01),烟曲霉处理组也出现细胞跨膜电阻值的显著下降(P<0.01)。与单独烟曲霉处理组比较,SB203580(20μmol/L,p38 MAPK抑制剂)干预组、Y27632(20μmol/L,ROCK抑制剂)干预组以及LY317615(10μmol/L,蛋白激酶C抑制剂)干预组的跨膜电阻值均显著上升(P<0.05)。结论烟曲霉处理致肺微血管内皮细胞通透性增加,其机制可能涉及p38 MAPK、ROCK激酶以及蛋白激酶C通路。
Objective To investigate the effect of Aspergillus fumigatus（ AF） on human pulmonary microvascular endothelial cell（ HPMVEC） permeability and the related mechanisms.Methods HPMVECs were treated with AF, cell F-actin was observed with confocal laser scanning microscopy and cell transmembrane resistance was measured. In addition, the cell permeability changes in AF-treated HPMVECs were also examined with intervention of p38 MAPK inhibitor SB203580（ 20 μmol/L）,ROCK inhibitor Y27632（ 20 μmol/L）,or PKC inhibitor LY317615（ 10 μmol/L）,respectively. Results AF treatment induced a significant reduction of Factin fluorescence intensity（ P〈0.01） and a significant reduction of cell transmembrane resistance（ P〈0.01） in HPMVECs. Furthermore,treatment with SB203580,Y27632 or LY317615 significantly inhibited（ P〈0.05） AF-induced increase of cell transmbrane resistance in HPMVECs. Conclusion AF can increase cell permeability in HMVECs,in which the MAPK（ p38）,ROCK and PKC pathways may be involved.
作者
宋珺
韩菁
孙越
施伟民
SONG Jun;HAN Jing;SUN Yue;SHI Wei-min(Dept.of Dermatology,First People＇s Hospital,Shanghai Jiao Tong University,Shanghai 200080,China)
出处
《同济大学学报（医学版）》
CAS
2018年第3期19-23,共5页
Journal of Tongji University(Medical Science)
基金
国家重点基础研究发展计划(973计划)(2013CB531604)
上海交通大学附属第一人民医院院级项目(11B06)
关键词
烟曲霉
肺微血管内皮细胞
细胞通透性
Aspergillus fumigatus
pulmonary microvascular endothelial cells
cell permeability
