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首页> 外文期刊>Cellular Physiology and Biochemistry >Attenuation of Glomerular Endothelial Cells from High Glucose-Induced Injury by Blockade of MAD2B
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Attenuation of Glomerular Endothelial Cells from High Glucose-Induced Injury by Blockade of MAD2B

机译：高糖诱导的MAD2B阻断导致肾小球内皮细胞的衰减

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>Background/Aims: To assess the role of mitotic arrest-deficient 2-like protein 2 (MAD2B) in high glucose-induced injury in mouse glomerular endothelial cells (GEnCs). Methods: GEnCs were cultured in vitro, and MAD2B protein levels were measured by Western blot in cells stimulated with high glucose (30 mM) for various periods of time. MAD2B and scrambled shRNA were introduced into GEnCs by liposomal transfection. Cell proliferation, apoptosis, nitric oxide (NO) production, and monolayer permeability were then measured in cells grown in the following conditions: control, high glucose treatment, MAD2B shRNA transfection with high glucose treatment, and scrambled shRNA transfection with high glucose treatment. Results: High glucose increased the protein levels of MAD2B in GEnCs. Compared with control cells, apoptosis was increased by high glucose treatment, which was attenuated by transfection with MAD2B shRNA transfection. Cells treated with high glucose produced less NO than control cells, whereas MAD2B shRNA transfection increased NO production. Cell monolayer permeability was enhanced in high glucose treated cells, but MAD2B shRNA transfection reduced permeability. Conclusion: High glucose levels induced the expression of MAD2B in GEnCs, whereas suppressing its expression reduced high glucose-induced endothelial cell apoptosis and high permeability, and promoted cell proliferation and NO production.
机译：> 背景/目的： 评估有丝分裂阻滞缺陷2样蛋白2（MAD2B）在高糖诱导的小鼠肾小球内皮细胞损伤中的作用（ GEnC）。 方法： GEnCs进行了体外培养，通过蛋白质印迹法检测了高葡萄糖（30 mM）刺激的各种细胞的MAD2B蛋白水平。时间段。通过脂质体转染将 MAD2B 和加扰的shRNA导入GEnC。然后在以下条件下生长的细胞中测量细胞增殖，凋亡，一氧化氮（NO）产生和单层通透性：对照，高葡萄糖处理，采用高葡萄糖处理的 MAD2B shRNA转染和加扰的shRNA高糖转染治疗。 结果： 高血糖会增加GEnC中MAD2B的蛋白水平。与对照细胞相比，高糖处理可增加细胞凋亡，而 MAD2B shRNA转染可减轻细胞凋亡。用高葡萄糖处理的细胞产生的NO少于对照细胞，而 MAD2B shRNA转染增加了NO的产生。在高葡萄糖处理的细胞中，细胞单层通透性增强，但是 MAD2B shRNA转染降低了通透性。 结论： 高糖水平诱导GEnCs中MAD2B的表达，而抑制它的表达降低了高糖诱导的内皮细胞凋亡和高通透性，并促进了细胞增殖和NO的产生。

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