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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Glial cell-derived neurotrophic factor protects against proteasome inhibition-induced dopamine neuron degeneration by suppression of endoplasmic reticulum stress and caspase-3 activation.
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Glial cell-derived neurotrophic factor protects against proteasome inhibition-induced dopamine neuron degeneration by suppression of endoplasmic reticulum stress and caspase-3 activation.

机译：胶质细胞源性神经营养因子通过抑制内质网应激和caspase-3活化来防止蛋白酶体抑制诱导的多巴胺神经元变性。

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Evidence has shown that ubiquitin proteasome system (UPS) impairment plays an important role in the dopamine (DA) neurodegeneration in Parkinson's disease (PD). It has been reported that application of proteasomal inhibitor lactacystin in ventral mesencephalon (VM) cultures can cause DA neurodegeneration, although the underlying mechanisms are not clear. Herein, we used the lactacystin-induced DA cell degeneration model to study the neuroprotection of glial cell-derived neurotrophic factor (GDNF) in VM cultures. We measured the expression of endoplasmic reticulum stress (ERS)-related genes, and determined the caspase-3 activation, apoptotic cell death, as well as alpha-synuclein-positive inclusions in DA neurons. We found that GDNF treatment significantly suppressed the expression of ERS-related genes and inhibited the activation of caspase-3 and apoptotic cell death without affecting alpha-synuclein-positive inclusions in DA neurons. Our study suggests that the protection of GDNF against DA neurodegeneration in the UPS impairment model is associated with ERS and caspase-3 suppression.
机译：有证据表明，泛素蛋白酶体系统（UPS）损伤在帕金森氏病（PD）的多巴胺（DA）神经退行性变中起重要作用。据报道，尽管腹腔中脑（VM）培养中使用蛋白酶体抑制剂lacticacystin可引起DA神经变性，但其潜在机制尚不清楚。在这里，我们使用了lactyacystin诱导的DA细胞变性模型来研究VM培养物中神经胶质细胞源性神经营养因子（GDNF）的神经保护作用。我们测量了内质网应激（ERS）相关基因的表达，并确定了caspase-3激活，凋亡细胞死亡以及DA神经元中的α-突触核蛋白阳性包涵体。我们发现，GDNF处理可显着抑制ERS相关基因的表达，并抑制caspase-3的激活和凋亡细胞死亡，而不会影响DA神经元中的α-突触核蛋白阳性包涵体。我们的研究表明，UPS损伤模型中GDNF对DA神经变性的保护与ERS和caspase-3抑制有关。

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