Calcium Dobesilate Inhibits the Oxidative Damage of Müller Cells Induced by High-glucose via the AQP4/Kir4.1 Axis
10.11969/j.issn.1673-548X.2025.06.009
- VernacularTitle:羟苯磺酸钙通过AQP4/Kir4.1轴抑制高糖诱导的Müller细胞氧化损伤的机制研究
- Author:
Xuewei QIN
1
;
Limin WANG
1
;
Xianfeng YAO
1
Author Information
1. 550001 贵阳,贵州中医药大学第一附属医院眼科
- Publication Type:Journal Article
- Keywords:
Calcium dobesilate;
Muller cells;
Oxidative damage;
AQP4/Kir4.1 axis
- From:
Journal of Medical Research
2025;54(6):44-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and mechanism of calcium dobesilate on oxidative damage induced by high-glucose in Müller cells.Methods The oxidative damage model of Müller cells induced by high-glucose was established and the cells were divided into 4groups.The control group was cultured normally,and the high glucose group was cultured in the medium of 35mmol/L glucose.The control+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of routine culture,and the high sugar+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of high glucose.Cell proliferation was assessed by CCK-8,apoptosis was detected by flow cytometry,and oxidative stress markers were detected by the kit.Intracellular correction potassium channel subtype 4.1(Kir4.1)and aquaporin 4(AQP4)protein levels were detected by western blot.Results Compared with the control group,the proliferative activity of Müller cells of the high glucose group was decreased,apoptosis rate was increased,oxidative stress occurred,AQP4 protein expression level was increased and Kir4.1 protein level was decreased(P＜0.05).Compared with the high glucose group,the cell activity and apoptosis rate of the high glucose+calcium do-besilate group were increased,the oxidative stress damage was alleviated,the AQP4 protein expression level was decreased and the Kir4.1 protein level was increased(P＜0.05).Conclusion Calcium dobesilate may inhibit the oxidative damage of Müller cells induced by high-glucose by regulating the AQP4/Kir4.1 axis.
