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Transplantation of human amniotic cells exerts neuroprotection in MPTP-induced Parkinson disease mice.

机译:人羊膜细胞移植在MPTP诱发的帕金森病小鼠中发挥神经保护作用。

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摘要

To determine the survival and differentiation of cultured Human amniotic cells (HACs) upon transplantation into the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson disease (PD) mice. Mouse model of PD was established with injections of MPTP (15 mg/kg, fourth, 2 h interval). After being labeled with PKH26, HACs isolated from human were transplanted into the striatum of PD mice. Immunohistochemistry was performed to evaluate the toxicity of MPTP in the substantia nigra, graft survival and endogenous neurogenesis. Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) level in the striatum were tested by ELISA. Our results showed that cultured HACs can express the marker of neural progenitor cells and differentiate into neuron, dopaminergic neuron, astrocyte and oligodendrocyte. TH-positive neural cells were significantly reduced in the substantia nigra in the model mice, whereas which increased in transplantation mice. Immunohistology results showed that transplanted HACs survived and migrated in the brain of PD model mouse, though no morphological integration was observed. BrdU-positive cells in the Subventricular zone (SVZ) and neurotrophins of the striatum increased in the transplantation mice. The results suggested that transplanted HACs could survive and promote the endogenous neurogenesis of mice, which maybe related to the increased level of neurotrophins of the striatum.
机译:若要确定在移植的1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的帕金森病(PD)小鼠的大脑中培养的人类羊膜细胞(HACs)的存活和分化。通过注射MPTP(15 mg / kg,第4、2 h间隔)建立PD的小鼠模型。用PKH26标记后,将从人分离的HAC移植到PD小鼠的纹状体中。进行了免疫组织化学,以评估MPTP对黑质,移植物存活和内源性神经发生的毒性。通过ELISA检测纹状体中脑源性神经营养因子(BDNF)和胶质细胞系源性神经营养因子(GDNF)的水平。我们的结果表明,培养的HAC可以表达神经祖细胞的标志物,并分化为神经元,多巴胺能神经元,星形胶质细胞和少突胶质细胞。在模型小鼠的黑质中,TH阳性神经细胞明显减少,而在移植小鼠中则增加。免疫组织学结果表明,移植的HACs在PD模型小鼠的脑中存活并迁移,尽管未观察到形态学整合。在移植小鼠中,脑室下区(SVZ)的BrdU阳性细胞和纹状体的神经营养蛋白增加。结果表明,移植的HACs可以存活并促进小鼠的内源性神经发生,这可能与纹状体的神经营养蛋白水平升高有关。

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