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Bone Marrow-Derived Mesenchymal Stem Cells Improve the Functioning of Neurotrophic Factors in a Mouse Model of Diabetic Neuropathy

机译:骨髓源性间充质干细胞改善糖尿病性神经病小鼠模型中神经营养因子的功能

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摘要

Diabetic neuropathy is one of the most frequent and troublesome complications of diabetes. Although there has been a continuous increase in the incidence of diabetic neuropathy, treatments have yet to be found that effectively treat diabetic neuropathy. Neurotrophic factors are proteins that promote the survival of specific neuronal populations. They also play key roles in the regeneration of peripheral nervous system. Recent evidence from diabetic animal models and human diabetic subjects suggest that reduced availability of neurotrophic factors may contribute to the pathogenesis of diabetic neuropathy. One way to reverse this effect is to take advantage of the finding that bone marrow derived mesenchymal stem cells (BM-MSCs) promote peripheral nerve repair and the functioning of neurotrophic factors. Therefore, we speculated that treatment with BM-MSCs could be a viable therapeutic strategy for diabetic neuropathy. The present study was designed to examine the possible beneficial effect of BM-MSCs on functions of neurotrophic factors in diabetic neuropathy. To assess this possibility, we used an in vivo streptozotocin-induced diabetic neuropathy mouse model. Quantitative real-time polymerase-chain reacion showed that BM-MSCs significantly increase expression levels of neurotrophic factors. Also, BM-MSCs ameliorated nerve conduction velocity in streptozotocin-treated mice. These results may help to elucidate the mechanism by which BM-MSCs function as a cell therapy agent in diabetic neuropathy.
机译:糖尿病性神经病是糖尿病最常见和最麻烦的并发症之一。尽管糖尿病性神经病的发生率持续增加,但是尚未发现有效治疗糖尿病性神经病的治疗方法。神经营养因子是促进特定神经元种群存活的蛋白质。它们在周围神经系统的再生中也起着关键作用。糖尿病动物模型和人类糖尿病患者的最新证据表明,神经营养因子的可用性降低可能与糖尿病性神经病的发病机理有关。逆转这种影响的一种方法是利用发现骨髓衍生的间充质干细胞(BM-MSC)促进周围神经修复和神经营养因子功能的发现。因此,我们推测用BM-MSCs治疗可能是糖尿病性神经病的可行治疗策略。本研究旨在检查BM-MSC对糖尿病性神经病中神经营养因子功能的可能有益作用。为了评估这种可能性,我们使用了体内链脲佐菌素诱导的糖尿病神经病变小鼠模型。实时定量聚合酶链反应显示,BM-MSC可显着增加神经营养因子的表达水平。而且,BM-MSC改善了链脲佐菌素处理的小鼠的神经传导速度。这些结果可能有助于阐明BM-MSC在糖尿病性神经病中作为细胞治疗剂发挥作用的机制。

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