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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Isosteviol Sodium Protects Neural Cells Against Hypoxia-Induced Apoptosis Through Inhibiting MAPK and NF-κB Pathways
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Isosteviol Sodium Protects Neural Cells Against Hypoxia-Induced Apoptosis Through Inhibiting MAPK and NF-κB Pathways

机译：Isosteviol钠通过抑制MAPK和NF-κB途径来保护神经细胞免受缺氧诱导的细胞凋亡

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BackgroundStevioside, isolated from the herbStevia rebaudiana, has been widely used as a food sweetener all over the world. Isosteviol Sodium (STV-Na), an injectable formulation of isosteviol sodium salt, has been proved to possess much greater solubility and bioavailability and exhibit protective effects against cerebral ischemia injury in vivo by inhibiting neuron apoptosis. However, the underlying mechanisms of the neuroprotective effects STV-Na are still not completely known. In the present study, we investigated the effects of STV-Na on neuronal cell death caused by hypoxia in vitro and its underlying mechanisms. MethodsWe used cobalt chloride (CoCl2) to expose mouse neuroblastoma N2a cells to hypoxic conditions in vitro. ResultsOur results showed that pretreatment with STV-Na (20 μM) significantly attenuated the decrease of cell viability, lactate dehydrogenase release and cell apoptosis under conditions of CoCl2-induced hypoxia. Meanwhile, STV-Na pretreatment significantly attenuated the upregulation of intracellular Ca2+concentration and reactive oxygen species production, and inhibited mitochondrial depolarization in N2a cells under conditions of CoCl2-induced hypoxia. Furthermore, STV-Na pretreatment significantly downregulated expressions of nitric oxide synthase, interleukin-1β, tumor necrosis factor-α, interleukin-6, nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signalings in N2a cells under conditions of CoCl2-induced hypoxia. ConclusionsTaken together, STV-Na protects neural cells against hypoxia-induced apoptosis through inhibiting MAPK and NF-κB pathways.
机译：BackgroundStevioside来自Herbstevia Rebaudiana，已被广泛用作全世界的食品甜味剂。已经证明，蛇硫醇钠（STV-NA），蛇硫醇钠盐的可注射制剂，通过抑制神经元凋亡，具有更大的溶解性和生物利用度，并对体内脑缺血损伤表现出保护作用。然而，神经保护作用的根本机制STV-NA仍然没有完全已知。在本研究中，我们研究了STV-NA对体外缺氧引起的神经细胞死亡的影响及其潜在机制。方法网络使用氯化钴（COCl2）将小鼠神经母细胞瘤N2A细胞暴露于体外缺氧条件。结果结果表明，在COCL2诱导的缺氧的条件下，具有STV-NA（20μm）的预处理显着减弱了细胞活力，乳酸脱氢酶释放和细胞凋亡的降低。同时，STV-NA预处理显着减弱了细胞内Ca2 +浓度和反应性氧物质生产的上调，并在CoCl2诱导的缺氧条件下抑制N2A细胞中的线粒体去极化。此外，在N2A中，STV-NA预处理明显下调了一氧化氮合酶，白细胞介素-1β，肿瘤坏死因子-α，白细胞介素-6，核因子Kappa（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号细胞在Cocl2诱导的缺氧的条件下。结论在一起，STV-NA通过抑制MAPK和NF-κB途径来保护神经细胞免受缺氧诱导的细胞凋亡。

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