Relationship between annexin 1 and endogenous protective mechanism during intestinal epithelial cell injury induced by endotoxin
10.3760/cma.j.issn.0254-1416.2016.04.032
- VernacularTitle:膜联蛋白A1与内毒素致肠上皮细胞损伤时内源性保护机制的关系
- Author:
Xi CHEN
;
Xiaohua GUO
;
Yongying PAN
;
Xingrong SONG
- Publication Type:Journal Article
- Keywords:
ANXA1;
Endotoxins;
Intestines;
Epithelial cells
- From:
Chinese Journal of Anesthesiology
2016;36(4):501-504
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the relationship between annexin 1 (ANXA1) and the endogenous protective mechanism during intestinal epithelial cell injury induced by endotoxiu.Methods The intestinal epithelial cells at the logarithmic growth phase were seeded in culture palates and randomly divided into 4 groups (n =36 each) using a random number table:control group (group C),cell injury group (group I),ANXA1 overexpression group (group OE),and ANXA1 silencing group (group S).Lentivirus with ANXA1 overexpression and silencing was transfected into intestinal epithelial cells to construct a stable cell line.In I,OE and S groups,endotoxin was added with the final concentration of 100 μg/ml,and the cells were then incubated for 24 h to establish the cell injury model.The culture medium was changed,and the cells were then incubated for 24 h in group C.The cell apoptosis was detected by flow cytometry,the cell permeability was determined by Transwell assay,and the cell viability was evaluated by methyl thiazolyl tetrazolium assay.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,and the cell permeability and viability were significantly decreased in I,OE and S groups (P＜0.05).Compared with group Ⅰ,the apoptosis rate was significantly decreased,the cell permeability and viability were significantly increased in group OE,and the apoptosis rate was significantly increased,and the cell permeability and viability were significantly decreased in group S (P＜0.05).Conclusion ANXA1 is involved in the endogenous protective mechanism during intestinal epithelial cell injury induced by endotoxin.
