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Granulocyte-colony stimulating factor is involved in low-dose LPS-induced neuroprotection.

机译:粒细胞集落刺激因子参与低剂量LPS​​诱导的神经保护作用。

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摘要

Granulocyte-colony stimulating factor (G-CSF) has recently been noted for neuroprotective function. Evidence has been given to indicate that G-CSF is naturally expressed in neurons and directly activates anti-apoptosis pathways. Finding out the agents inducing G-CSF production is of value for understanding the neuroprotection network in central nervous system. It is known that lipopolysaccharide (LPS) can induce macrophages to produce G-CSF. Here we demonstrate that hippocampal neurons exhibited the expression of toll-like receptor-4, and prove that low-dose LPS treatment increased the expression and production of G-CSF mRNA and protein in cultured neurons. We further indicate that the neutralization of G-CSF with corresponding anti-G-CSF antibodies abolished the neuroprotective effect of LPS pretreatment in N-methyl-D-aspartic acid-induced neuronal injury by MTT/CCK-8 assays and LDH release. Thus our results reveal that G-CSF may be involved in LPS-mediated neuroprotection in vivo.
机译:最近已经注意到粒细胞集落刺激因子(G-CSF)具有神经保护功能。已有证据表明,G-CSF在神经元中自然表达并直接激活抗凋亡途径。找出诱导G-CSF产生的药物对于理解中枢神经系统的神经保护网络具有重要的价值。已知脂多糖(LPS)可诱导巨噬细胞产生G-CSF。在这里,我们证明海马神经元表现出toll样受体4的表达,并证明低剂量LPS​​处理可提高培养的神经元中G-CSF mRNA和蛋白的表达和产生。我们进一步表明,用相应的抗G-CSF抗体中和G-CSF消除了LPS预处理在N-甲基-D-天冬氨酸诱导的MTT / CCK-8分析和LDH释放引起的神经元损伤中的神经保护作用。因此,我们的结果表明,G-CSF可能参与体内LPS介导的神经保护。

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