| 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 |
| 投稿时间：2024-12-06 修订日期：2025-01-06 点此下载全文 |
| 引用本文：秦学维,王利民,姚贤凤,陈梅,郑开金,郑丽.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[J].医学研究杂志,2025,54(6):44-48 |
| DOI：
10.11969/j.issn.1673-548X.2025.06.009 |
| 摘要点击次数: 19 |
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| 基金项目:国家自然科学基金资助项目(82060886)；贵州省自然科学基金资助项目｛黔科合基础[2020]1Y366｝；贵州省中医药管理局中医药、民族医药科学技术研究专项课题资助项目(QZYY-2019-005) |
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| 中文摘要:目的 研究羟苯磺酸钙在高糖诱导的环境下对Müller细胞氧化损伤的保护作用及其机制。方法 通过高糖诱导建立Müller细胞氧化损伤模型,并将细胞分为4组,即对照组(正常培养)、高糖组(35mmol/L葡萄糖培养基)、对照+羟苯磺酸钙组(常规培养基础上加入0.5μmol/L羟苯磺酸钙)和高糖+羟苯磺酸钙组(高糖基础上加入0.5μmol/L羟苯磺酸钙)。使用CCK-8评估细胞增殖,流式细胞术检测细胞凋亡,试剂盒检测氧化应激指标,蛋白印迹技术检测内向整流钾离子通道4.1(inwardly rectifying K channel 4.1,Kir4.1)和水通道蛋白4(aquaporin-4,AQP4)蛋白水平。结果 与对照组比较,高糖组Müller细胞增殖活性降低且凋亡率升高,细胞发生氧化应激,AQP4蛋白表达水平升高而Kir4.1蛋白表达水平降低(P<0.05)。与高糖组比较,高糖+羟苯磺酸钙组细胞增殖活性增加且凋亡率降低,细胞氧化应激损伤减轻,AQP4蛋白表达水平降低而Kir4.1蛋白表达水平升高(P<0.05)。结论 羟苯磺酸钙可能通过调节AQP4/Kir4.1轴抑制高糖诱导的Müller细胞氧化损伤。 |
| 中文关键词:羟苯磺酸钙 Müller细胞 氧化损伤 AQP4/Kir4.1轴 |
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| Calcium Dobesilate Inhibits the Oxidative Damage of Müller Cells Induced by High-glucose via the AQP4/Kir4.1 Axis. |
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| 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 dobesilate 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. |
| keywords:Calcium dobesilate Muller cells Oxidative damage AQP4/Kir4.1 axis |
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