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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Baicalein inhibits alpha-synuclein oligomer formation and prevents progression of alpha-synuclein accumulation in a rotenone mouse model of Parkinson's disease
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Baicalein inhibits alpha-synuclein oligomer formation and prevents progression of alpha-synuclein accumulation in a rotenone mouse model of Parkinson's disease

机译：黄ical素抑制帕金森氏病鱼藤酮小鼠模型中α-突触核蛋白低聚物的形成并阻止α-突触核蛋白积聚的进程

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Parkinson's disease (PD) is a progressive neurodegenerative disease. alpha-Synuclein (alpha-syn) oligomers play a critical role in the progression of PD. Baicalein, a typical flavonoid compound, can inhibit the formation of the alpha-syn oligomers, and disaggregate existing alpha-syn oligomers in vitro. However, whether baicalein could inhibit or disaggregate alpha-syn oligomers in vivo has not been investigated. Therefore, this study was designed to investigate the inhibitory effects of baicalein on alpha-syn oligomers in vivo and to explore the possible mechanisms of such inhibition. A chronic PD mouse model was created by continuous intragastric administration of rotenone (5 mg/kg, 12 weeks). Baicalein (100 mg/kg) was intraperitoneally injected from 7 week to 12 week. Our result showed that the amount of a-syn, changes in the levels of the striatal neurotransmitters, and the behavioral changes found in the chronic PD mouse model were prevented after the baicalein injections. Although baicalein did not decrease alpha-syn mRNA expression, alpha-syn oligomers were significantly decreased in the ileum, thoracic spinal cord, and midbrain. Furthermore, transmission electron microscopy analysis showed that baicalein could prevent alpha-syn monomers from the oligomer formation in vitro. Taken together, these results suggest that baicalein could prevent the progression of a-syn accumulation in PD mouse model partly by inhibiting formation of the a-syn oligomers. (C) 2016 Elsevier B.V. All rights reserved.
机译：帕金森氏病（PD）是一种进行性神经退行性疾病。 α-突触核蛋白（α-syn）低聚物在PD的进展中起关键作用。黄ical素是一种典型的类黄酮化合物，可以抑制α-syn寡聚物的形成，并在体外分解现有的α-syn寡聚物。然而，黄ical素是否可以在体内抑制或分解α-syn寡聚物。因此，本研究旨在研究黄ical素对体内α-syn寡聚物的抑制作用，并探讨这种抑制作用的可能机制。通过连续胃内注射鱼藤酮（5 mg / kg，12周）来创建慢性PD小鼠模型。从第7周到第12周腹膜内注射黄ical素（100 mg / kg）。我们的结果表明，在黄ical素注射后，可以预防a-syn的量，纹状体神经递质水平的变化以及在慢性PD小鼠模型中发现的行为变化。尽管黄ical素不降低α-synmRNA的表达，但在回肠，胸脊髓和中脑中α-syn寡聚体明显减少。此外，透射电子显微镜分析表明，黄ical苷可以在体外阻止α-syn单体形成低聚物。两者合计，这些结果表明黄ical素可以部分通过抑制a-syn寡聚体的形成来阻止PD小鼠模型中a-syn积累的进展。 （C）2016 Elsevier B.V.保留所有权利。

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