Therapeutic Effect of Padina arborescens Extract on a Cell System Model for Parkinson's Disease.

IF 1.6 Q3 CLINICAL NEUROLOGY NeuroSci Pub Date : 2024-08-30 eCollection Date: 2024-09-01 DOI:10.3390/neurosci5030024
Dong Hwan Ho, Hyejung Kim, Daleum Nam, Mi Kyoung Seo, Sung Woo Park, Dong-Kyu Kim, Ilhong Son
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Abstract

Leucine-rich repeat kinase 2 (LRRK2) and α-synuclein are involved in the pathogenesis of Parkinson's disease. The activity of LRRK2 in microglial cells is associated with neuroinflammation, and LRRK2 inhibitors are crucial for alleviating this neuroinflammatory response. α-synuclein contributes to oxidative stress in the dopaminergic neuron and neuroinflammation through Toll-like receptors in microglia. In this study, we investigated the effect of the marine alga Padina arborescens on neuroinflammation by examining LRRK2 activation and the aggregation of α-synuclein. P. arborescens extract inhibits LRRK2 activity in vitro and decreases lipopolysaccharide (LPS)-induced LRRK2 upregulation in BV2, a mouse microglial cell line. Treatment with P. arborescens extract decreased tumor necrosis factor-α (TNF-α) gene expression by LPS through LRRK2 inhibition in BV2. It also attenuated TNF-α gene expression, inducible nitric oxide synthase, and the release of TNF-α and cellular nitric oxide in rat primary microglia. Furthermore, P. arborescens extract prevented rotenone (RTN)-induced oxidative stress in primary rat astrocytes and inhibited α-synuclein fibrilization in an in vitro assay using recombinant α-synuclein and in the differentiated human dopaminergic neuronal cell line SH-SY5Y (dSH). The extract increased lysosomal activity in dSH cells. In addition, P. arborescens extract slightly prolonged the lifespan of Caenorhabditis elegans, which was reduced by RTN treatment.

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Padina arborescens 提取物对帕金森病细胞系统模型的治疗效果
富亮氨酸重复激酶2(LRRK2)和α-突触核蛋白与帕金森病的发病机制有关。LRRK2 在小胶质细胞中的活性与神经炎症有关,而 LRRK2 抑制剂对于减轻这种神经炎症反应至关重要。α-突触核蛋白通过小胶质细胞中的 Toll 样受体,促进多巴胺能神经元的氧化应激和神经炎症。在这项研究中,我们通过检测 LRRK2 的激活和 α-突触核蛋白的聚集,研究了海洋藻类 Padina arborescens 对神经炎症的影响。石莲花提取物在体外能抑制 LRRK2 的活性,并能降低脂多糖(LPS)诱导的 LRRK2 在小鼠小胶质细胞系 BV2 中的上调。通过抑制小鼠微神经胶质细胞系 BV2 中的 LRRK2,用旱芹提取物处理可降低 LPS 诱导的肿瘤坏死因子-α(TNF-α)基因表达。它还能减少大鼠原代小胶质细胞中 TNF-α 基因表达、诱导型一氧化氮合酶以及 TNF-α 和细胞一氧化氮的释放。此外,旱金莲提取物还能防止鱼藤酮(RTN)诱导的原代大鼠星形胶质细胞氧化应激,并在使用重组α-突触核蛋白的体外试验中抑制α-突触核蛋白纤维化,以及在分化的人多巴胺能神经细胞系SH-SY5Y(dSH)中抑制α-突触核蛋白纤维化。提取物提高了 dSH 细胞的溶酶体活性。此外,旱金莲提取物还能轻微延长秀丽隐杆线虫的寿命,而 RTN 处理则会缩短秀丽隐杆线虫的寿命。
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