封堵器
脂多糖
原癌基因酪氨酸蛋白激酶Src
免疫印迹
紧密连接
激酶
化学
炎症
免疫荧光
细胞生物学
分子生物学
作者
Yong-Bin Han,Fazhan Zhang,Liyan Zhang,Shengfa Zheng,Gang Li,Hongxiu Liu,Tao Zhao
出处
期刊:International Journal of Anesthesiology and Resuscitation
[Chinese Medical Association]
日期:2016-12-15
卷期号:37 (12): 1089-1092
标识
DOI:10.3760/cma.j.issn.1673-4378.2016.12.007
摘要
Objective
To investigate the effect of c-Src kinase on the expression of the tight junction protein occludin during lipopolysaccharides (LPS) treatment on mouse lung epithelial-12(MLE-12) cells.
Methods
The cultured MLE-12 cells were randomly divided into 3 groups: control group (group C), LPS group (group L), LPS+c-Src kinase inhibitor (PP2) group (group L+P). In group L, MLE-12 cells were treated with LPS (10 mg/L) for 1, 3, 6 h, respectively. In group L+P, MLE-12 cells were treated with c-Src kinase inhibitor PP2 (100 μmol/L) for 30 min then LPS (10 mg/L) for 6h. Non-treatment was given in group C. The expression of occludin was determined in MLE-12 cells using Western blot and immunofluorescence.
Results
In our study, we found that compared with group C, the expression of occludin of group L was significantly down-regulated at 6 h (P<0.05) and c-Src was up-regulated (P<0.05). The expression of occludin was significantly up-regulated in group L+P (P<0.05) at 6 h compared with group L. Immunofluorescence showed that occludin which distributed in cytomembrane could be affected by LPS, and PP2 could alleviate the effect of LPS. And the level of occludin was increased after treated with PP2 in group L+P.
Conclusions
LPS leads to decreasing of the expression of occludin in MLE-12 cells, with c-Src involved in the process.
Key words:
c-Src kinase; Lipopolysaccharide; Tight Junctions; Occludin
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