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首页> 外文期刊>BioResearch open access. >Effect of BDNF and Other Potential Survival Factors in Models of In Vitro Oxidative Stress on Adult Spinal Cord–Derived Neural Stem/Progenitor Cells
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Effect of BDNF and Other Potential Survival Factors in Models of In Vitro Oxidative Stress on Adult Spinal Cord–Derived Neural Stem/Progenitor Cells

机译：BDNF和其他潜在存活因子在体外氧化应激模型中对成年脊髓源性神经干/祖细胞的影响

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Transplantation of neural stem/progenitor cells (NSPCs) is a promising strategy in spinal cord injury (SCI). However, poor survival of transplanted stem cells remains a major limitation of this therapy due to the hostile environment of the injured cord. Oxidative stress is a hallmark in the pathogenesis of SCI; however, its effects on NSPCs from the adult spinal cord have yet to be examined. We therefore developed in vitro models of mild and severe oxidative stress of adult spinal cord–derived NSPCs and used these models to examine potential cell survival factors. NSPCs harvested from the adult rat spinal cord were treated with hydrogen peroxide (H2O2) in vitro to induce oxidative stress. A mild 4?h exposure to H2O2 (500?μM) significantly increased the level of intracellular reactive oxygen species with minimal effect on viability. In contrast, 24?h of oxidative stress led to a marked reduction in cell survival. Pretreatment with brain-derived neurotrophic factor (BDNF) for 48?h attenuated the increase in intracellular reactive oxygen species and enhanced survival. This survival effect was associated with a significant reduction in the number of apoptotic cells and a significant increase in the activity of the antioxidant enzymes glutathione reductase and superoxide dismutase. BDNF treatment had no effect on NSPC differentiation or proliferation. In contrast, cyclosporin A and thyrotropin-releasing hormone had minimal or no effect on NSPC survival. Thus, these models of in vitro oxidative stress may be useful for screening neuroprotective factors administered prior to transplantation to enhance survival of stem cell transplants.
机译：神经干/祖细胞（NSPC）的移植是脊髓损伤（SCI）中的一种有前途的策略。然而，由于受伤的脐带的不利环境，移植的干细胞存活率低仍然是该疗法的主要限制。氧化应激是SCI发病机制的标志。然而，它对成年脊髓对NSPC的影响尚待研究。因此，我们开发了成年脊髓源性NSPC轻度和重度氧化应激的体外模型，并使用这些模型检查了潜在的细胞存活因子。用过氧化氢（H 2 O 2 ）处理从成年大鼠脊髓收获的NSPC，以诱导氧化应激。轻度4？h暴露于H 2 O 2 （500μM）会显着增加细胞内活性氧的水平，而对活力的影响最小。相比之下，24小时的氧化应激导致细胞存活率显着降低。用脑源性神经营养因子（BDNF）预处理48？h可减弱细胞内活性氧的增加并提高存活率。这种存活作用与凋亡细胞数量的显着减少以及抗氧化酶谷胱甘肽还原酶和超氧化物歧化酶的活性显着增加有关。 BDNF治疗对NSPC的分化或增殖没有影响。相反，环孢菌素A和促甲状腺激素释放激素对NSPC生存的影响很小或没有影响。因此，这些体外氧化应激模型可用于筛选在移植前给予的神经保护因子，以增强干细胞移植的存活率。

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