Interleukin-8 antagonist down regulates the adhesion and migration of retinal vascular endothelial cells by inhibiting the production of reactive oxygen species
10.3760/cma.j.cn511434-20220315-00148
- VernacularTitle:白细胞介素-8拮抗剂通过抑制活性氧生成下调视网膜血管内皮细胞黏附和迁移
- Author:
Linni WANG
1
;
Jingjing CAO
;
Dongjun XING
;
Rongguo YU
;
Liying HU
;
Yang YANG
;
Chang LI
;
Zhiqing LI
;
Hui LI
;
Yaru HONG
;
Lijie DONG
Author Information
1. 天津医科大学眼科医院、眼视光学院、眼科研究所 国家眼耳鼻喉疾病临床医学研究中心天津市分中心 天津市视网膜功能与疾病重点实验室，天津 300384
- Keywords:
Retinal vascular endothelial cells;
Interleukin-8;
Migration;
Adhesion;
Reactive Oxygen species;
Cell experiment
- From:
Chinese Journal of Ocular Fundus Diseases
2023;39(11):913-917
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effect of interleukin-8 (IL-8) on the adhesion and migration of retinal vascular endothelial cells (RCEC).Methods:A cell experiment. Human RCEC (hRCEC) was divided into normal control group (N group), advanced glycation end product (AGE) treatment group (AGE group), and AGE-induced combined IL-8 antagonist SB225002 treatment group (AGE+SB group). The effect of AGE on IL-8 expression in hRCEC was observed by Western blot. The effect of SB225002 on hRCEC migration was observed by cell scratch assay. The effects of SB225002 on leukocyte adhesion and reactive oxygen species (ROS) on hRCEC were detected by flow cytometry. Student- t test was performed between the two groups. Oneway analysis of variance was performed among the three groups. Results:Compared with group N, the expression level of IL-8 in cells of AGE group was significantly increased, with statistical significance ( t=25.661, P<0.001). Compared with N group and AGE+SB group, cell mobility in AGE group was significantly increased ( F=29.776), leukocyte adhesion number was significantly increased ( F=38.159, 38.556), ROS expression level was significantly increased ( F=22.336), and the differences were statistically significant ( P<0.05). Conclusion:IL-8 antagonist SB225002 may down-regulate hRCEC adhesion and migration by inhibiting ROS expression.
