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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Protection of MPTP-induced neuroinflammation and neurodegeneration by Pycnogenol
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Protection of MPTP-induced neuroinflammation and neurodegeneration by Pycnogenol

机译：碧萝ogen对MPTP诱导的神经炎症和神经变性的保护

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Oxidative stress and inflammation play a crucial role in Parkinson's disease (PD) pathogenesis and may represent a target for treatment. Current PD drugs provide only symptomatic relief and have limitations in terms of adverse effects and inability to prevent neurodegeneration. Flavonoids have been suggested to exert human health benefits by its anti-oxidant and anti-inflammatory properties. Therefore, in the present study, using 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine (MPTP)-induced mouse model of Parkinsonism, we investigated the neuroprotective potential of bioflavonoid compound Pycnogenol? (PYC), an extract of Pinus maritime bark. MPTP injected mice developed significantly severe oxidative stress and impaired motor coordination at day 1 and day 7 postinjection. This was associated with significantly increased inflammatory responses of astrocyte and microglia as assessed by ionized calcium binding adaptor molecule 1 (Iba 1) and glial fibrillary acidic protein (GFAP) immunohistochemistry, and nuclear transcription factor-κB (NF-κB), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in the striata by Western blot. Additionally, there was significant upregulation of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) expression in the striata of MPTP injected mice compared to saline controls. The MPTP-induced neuroinflammation, neurodegeneration and behavioral impairments were markedly repudiated by treatment with PYC. These results suggest that PYC protects dopaminergic neurons from MPTP-induced toxicity in the mouse model of PD. Thus, the present finding of PYC-induced adaptation to oxidative stress and inflammation could suggest a novel avenue for clinical intervention in neurodegenerative diseases including PD.
机译：氧化应激和炎症在帕金森氏病（PD）发病机理中起着至关重要的作用，可能代表治疗目标。当前的PD药物仅提供症状缓解，并且在副作用和不能预防神经变性方面具有局限性。已经建议类黄酮具有抗氧化和抗发炎的特性，对人体健康有益。因此，在本研究中，我们使用1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森氏症小鼠模型，研究了生物类黄酮化合物碧萝ogen的神经保护作用。 （PYC），松属海洋树皮的提取物。注射MPTP的小鼠在注射后的第1天和第7天出现明显的严重氧化应激并损害了运动协调性。通过离子钙结合衔接子分子1（Iba 1）和神经胶质纤维酸性蛋白（GFAP）免疫组化以及核转录因子-κB（NF-κB），诱导型一氧化氮评估，这与星形胶质细胞和小胶质细胞的炎症反应显着增加有关Western blot检测纹状体中合成酶（iNOS）和环氧合酶-2（COX-2）的表达。此外，与生理盐水对照组相比，MPTP注射的小鼠纹状体中肿瘤坏死因子-α（TNF-α）和白介素-1β（IL-1β）表达明显上调。通过PYC治疗可以明显地消除MPTP引起的神经炎症，神经退行性病变和行为障碍。这些结果表明，PYC保护多巴胺能神经元免受MPTP诱导的PD小鼠模型毒性的影响。因此，目前PYC诱导的对氧化应激和炎症的适应性发现可能为临床干预包括PD的神经退行性疾病提供了一条新途径。

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