首页> 外文期刊>Environmental toxicology and pharmacology >The bone marrow-derived mesenchymal stem cells (BMSCs) alleviate diabetic peripheral neuropathy induced by STZ via activating GSK-3β/β- catenin signaling pathway
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The bone marrow-derived mesenchymal stem cells (BMSCs) alleviate diabetic peripheral neuropathy induced by STZ via activating GSK-3β/β- catenin signaling pathway

机译:骨髓衍生的间充质干细胞(BMSCs)通过激活GSK-3β/β-连环素信号传导途径缓解STZ诱导的糖尿病外周神经病变

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摘要

Background: Diabetic peripheral neuropathy, a common complication of diabetic mellitus, has brought a threaten on patients' health. The bone marrow-derived mesenchymal stem cells (BMSCs) were reported to play an important role in diverse diseases. Nevertheless, the specific function of BMSCs in diabetic peripheral neuropathy remained uncharacterlzed. Methods: A wide range of experiments including RT-qPCR, western blot, H&E staining, oxidative stress assessment, measurement of thermal sensitivity, ELISA, urine protein and CCK-8 assays were implemented to explore the function and mechanism of BMSCs in vivo and vitro. Results: The experimental results displayed that BMSCs improve STZ-induced diabetes symptoms in rats by decreasing blood glucose and urinary protein. Functionally, BMSCs ameliorate oxidative stress, painful diabetic neuropathy, neurotrophic status and angiogenesis in STZ-induced rats. Moreover, BMSCs participate in the regulation of sciatic neuro morphology in diabetic neuropathy rat model. In mechanism, BMSCs alleviate diabetic peripheral neuropathy via activating GSK-3β/β-catenin signaling pathway in rats and improve Schwann's cells viability by activating GSK-3β/β-catenin signaling pathway under high glucose. Conclusions: We verified that BMSCs alleviate diabetic peripheral neuropathy of rats induced by STZ via activating GSK-3β/β-catenin signaling pathway, which implied a novel biomarker for diabetic peripheral neuropathy treatment.
机译:背景:糖尿病外周神经病变,糖尿病患者的常见并发症,对患者的健康带来了威胁。据报道,骨髓衍生的间充质干细胞(BMSCs)在不同的疾病中起重要作用。然而,BMSCs在糖尿病外周神经病变中的特异性功能仍然是无应的。方法:实施了诸如RT-QPCR,Western印迹,H&E染色,氧化应激评估,热敏性测量,ELISA,尿蛋白和CCK-8测定的各种实验,以探讨BMSCs在体内和体外的功能和机制。结果:通过减少血糖和泌尿蛋白,BMSCS展示BMSCS改善大鼠患者患者患者的症状。在功能上,BMSCs改善氧化应激,疼痛糖尿病神经病变,神经营养的状态和血管生成在STZ诱导的大鼠中。此外,BMSCS参与糖尿病神经病变大鼠模型中坐骨神经形态的调节。在机制中,BMSC通过激活大鼠GSK-3β/β-Catenin信号传导途径缓解糖尿病外周神经病变,通过激活高葡萄糖在高葡萄糖下激活GSK-3β/β-catenin信号传导途径来改善施万的细胞活力。结论:通过激活GSK-3β/β-Catenin信号通路,BMSCs缓解STZ诱导的大鼠的糖尿病外周神经病变,这暗示了一种用于糖尿病外周神经病理治疗的新型生物标志物。

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  • 来源
    《Environmental toxicology and pharmacology》 |2020年第10期|103432.1-103432.10|共10页
  • 作者单位

    Department of Orthopaedics The Second Affiliated Hospital of Nanchang University Nanchang 330008 Jiangxi China;

    Department of Cardiovascular Medicine The Second Affiliated Hospital of Nanchang University Nanchang 330008 Jiangxi China;

    Nanchang University Medical College Nanchang 330006 Jiangxi China;

    Jiujiang University Jiujiang 332005 Jiangxi China;

    Department of Endocrinology and Metabolism The Second Affiliated Hospital of Nanchang University Nanchang 330008 Jiangxi China;

    Department of Orthopaedics The Second Affiliated Hospital of Nanchang University Nanchang 330008 Jiangxi China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    BMSCs; Diabetic peripheral neuropathy; GSK-3β/β-catenin signaling pathway;

    机译:BMSCS;糖尿病外周神经病变;GSK-3β/β-Catenin信号通路;

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