Circ_0001953 contribute to retinal vascular endothelial cell injury induced by high glucose through regulating miR-186

被引:0
|
作者
Yuan, Yazhen [1 ]
Guan, Yongqing [1 ]
Shao, Chenjun [1 ]
Wang, Hui [2 ]
Zhang, Shuangmei [1 ]
机构
[1] Fourth Hosp Hebei Med Univ, Dept Ophthalmol, Shijiazhuang 050000, Hebei, Peoples R China
[2] Shijiazhuang peoples Hosp, Dept Ophthalmol, Shijiazhuang 050003, Hebei, Peoples R China
关键词
circ_0001953; miR-186; HRVECs; inflammation; oxidative stress; apoptosis; DIABETIC-RETINOPATHY; APOPTOSIS;
D O I
10.4314/tjpr.v22i3.13
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Purpose: To investigate the effects of circ_0001953/miR-186 on human retinal vascular endothelial cell (HRVEC) injury evoked by high glucose. Methods: A cell model (HG group) was established using high glucose-treated HRVECs, while untreated HRVECs were used as the control group (Con group). The levels of endothelin-1 (ET-1), ICAM-1 and IL-6 were evaluated by ELISA and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) in HRVECs were determined. Apoptosis rate was tested adopting flow cytometry. The interrelationship between circ_0001953 and miR-186 was assessed using dual luciferase reporter assay. Measurement of Bax and Bcl-2 was implemented via western blot. Results: In HG group, circ_0001953 increased while miR-186 was downregulated, ET-1, IL-6, ICAM-1, and apoptosis rate increased and accompanied with up-regulated Bax content and declined Bcl-2 protein level. Furthermore, the content of MDA increased and SOD decreased. MiR-186 was a target of circ_0001953. Conclusion: Inhibition of circ_0001953 can repress inflammation, oxidative stress and apoptosis in HRVECs by up-regulating the expression of miR-186.
引用
收藏
页码:563 / 569
页数:7
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