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首页> 外文期刊>Experimental and therapeutic medicine >Protective effect of astragalosides from Radix Astragali on adriamycin-induced podocyte injury
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Protective effect of astragalosides from Radix Astragali on adriamycin-induced podocyte injury

机译：黄芪中黄芪中黄芪诱导腺细胞损伤的保护作用

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Nephrotic syndrome (NS) is the most common kidney disease in clinical practice and may lead to end-stage renal failure. Astragalosides (AST) have been clinically tested for the treatment of NS, but their mechanism of action has remained to be elucidated. The aim of the present study was to investigate the effect of AST on the structure and function of podocytes with adriamycin (ADR)-induced damage and to elucidate the underlying molecular mechanisms. The mouse podocyte clone 5 (MPC5) immortalized mouse podocyte cell line was treated with 0.5 mu mol/l ADR to establish a podocyte injury model. The MPC5 podocytes were divided into a control group, a podocyte injury group and a low-, medium- and high-concentration AST treatment group. The results indicated that the survival rate of the podocyte injury group was significantly decreased compared with that in the control group and each AST-treated group had an increased survival rate compared with that in the podocyte injury group. Furthermore, each dose of AST significantly inhibited the ADR-associated increases the levels of lactate dehydrogenase and malondialdehyde and the decrease in the activity of superoxide dismutase in MPC5 podocytes. In addition, AST improved the migration ability of MPC5 podocytes and suppressed the cytoskeletal rearrangement associated with ADR-induced damage. Furthermore, matrix metalloproteinase (MMP)-2 and -9 were decreased in the podocyte injury group, which was inhibited by different concentrations of AST. Thus, AST was able to maintain the balance of oxidative. stress in podocytes cultured with ADR and protect them from ADR-induced injury. The mechanism may be associated with the upregulation of MMPs
机译：肾病综合征（NS）是临床实践中最常见的肾病，可能导致终末期肾功能衰竭。黄芪（AST）已被临床测试用于治疗NS，但它们的作用机制仍然被阐明。本研究的目的是探讨AST对具有亚霉素（ADR）诱导的损伤的诱饵结构和功能的影响，并阐明潜在的分子机制。用0.5μmol/ L ADR处理小鼠泛孔细胞克隆5（MPC5）永生化小鼠泛细胞细胞系以建立致孔细胞损伤模型。将MPC5致缩粒细胞分为对照组，致孔损伤组和低，中和高浓度ASS AST治疗组。结果表明，与对照组相比，泛骨细胞损伤组的存活率显着降低，并且每个AST治疗组的存活率增加了与泛细胞损伤组相比增加。此外，每剂AST显着抑制ADR相关增加乳酸脱氢酶和丙二醛水平，以及MPC5诱饵中超氧化物歧化酶的活性降低。此外，AST改善了MPC5孔细胞的迁移能力，并抑制了与ADR诱导的损伤相关的细胞骨骼重排。此外，在胆细胞损伤基团中降低了基质金属蛋白酶（MMP）-2和-9，其被不同浓度的AST抑制。因此，AST能够保持氧化的平衡。用ADR培养的诱导诱导诱导诱导损伤的诱导损伤的压力。该机制可能与MMP的上调相关联

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