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Biological Membrane-Packed Mesenchymal Stem Cells Treat Acute Kidney Disease by Ameliorating Mitochondrial-Related Apoptosis

机译:生物膜包装的间充质干细胞通过减轻线粒体相关的细胞凋亡治疗急性肾脏疾病

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摘要

The mortality of rhabdomyolysis-induced AKI remains high because no effective therapy exists. We investigated a new therapeutic method using MSCs. The aim of this study was to investigate the therapeutic potential and anti-apoptotic mechanisms of action of MSCs in the treatment of AKI induced by glycerol in vivo and in vitro. We used Duragen as a biological membrane to pack MSCs on the glycerol-injured renal tissue in vivo. The anti-apoptotic mechanism was investigated. In vitro, HK-2 cells were incubated with ferrous myoglobin and MSCs-conditioned medium, followed by cell proliferation and apoptosis assays. We founded that packing MSCs on the injured renal tissue preserved renal function, ameliorated renal tubular lesions, and reduced apoptosis in the mice with glycerol-induced AKI. The MSC-conditioned medium improved HK-2 cell viability and inhibited apoptosis. These effects were reversed by the PI3K inhibitor . Biological membrane packing of MSCs on the renal tissue has a therapeutic rescue function by inhibiting cell apoptosis in vivo. MSCs protect renal cells from apoptosis induced by myoglobin in vitro. We have thus demonstrated MSCs reduced rhabdomyolysis-associated renal injury and cell apoptosis by activating the PI3K/Akt pathway and inhibiting apoptosis.
机译:由于没有有效的治疗方法,横纹肌溶解引起的AKI的死亡率仍然很高。我们研究了一种使用MSC的新治疗方法。这项研究的目的是在体内和体外研究MSC在治疗AKI诱导的AKI中的治疗潜力和抗凋亡机制。我们将杜拉根(Duragen)用作生物膜,将MSCs包装在体内甘油受损的肾组织上。研究了抗凋亡机制。在体外,HK-2细胞与亚铁肌红蛋白和MSCs条件培养基一起孵育,然后进行细胞增殖和凋亡测定。我们发现,在受伤的肾脏组织上堆积MSC可以保留甘油诱导的AKI小鼠的肾功能,改善肾小管病变并减少细胞凋亡。 MSC条件培养基可改善HK-2细胞的活力并抑制细胞凋亡。这些作用被PI3K抑制剂逆转。 MSCs在肾脏组织上的生物膜堆积通过抑制体内细胞凋亡而具有治疗性抢救功能。 MSC保护肾细胞免受肌红蛋白在体外诱导的凋亡。因此,我们证明了MSC通过激活PI3K / Akt通路并抑制细胞凋亡来减少横纹肌溶解相关的肾损伤和细胞凋亡。

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