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首页> 外文期刊>RSC Advances >Ameliorative effects and possible molecular mechanisms of action of fibrauretine from Fibraurea recisa Pierre on d-galactose/AlCl3-mediated Alzheimer's disease
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Ameliorative effects and possible molecular mechanisms of action of fibrauretine from Fibraurea recisa Pierre on d-galactose/AlCl3-mediated Alzheimer's disease

机译：来自纤维雷的纤维雷的纤维素recisa pierre对D-半乳糖/ Alcl3介导的阿尔茨海默病疾病的改善效果及可能的分子机制

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摘要

Fibrauretine is one of the main active ingredients from the rattan stems of Fibraurea recisa Pierre It exhibits a series of significant pharmacological effects. The present study aimed to evaluate the potential anti Alzheimer's disease (AD) effects of fibrauretine on a d-galactose/AlCl3-induced mouse model, and the underlying mechanisms of action were further investigated for the first time. Our results showed that pretreatment with fibrauretine significantly improved the ability of spatial short-term working memory in the model mice during the Y-maze test, as well as the abilities of spatial learning and memory during the Morris water maze. The levels of brain tissue amyloid (A), P-Tau, Tau and acetylcholinesterase (AchE) were evidently increased in d-galactose/AlCl3-intoxicated mice, and these effects were reversed by fibrauretine. In contrast, a significant increase in the levels of the neurotransmitter acetylcholine (Ach) and choline acetyl transferase (ChAT) was observed in the fibrauretine-treated groups compared with the model group. Neuronal oxidative stress, evidenced by increased malondialdehyde (MDA) and nitric oxide (NO) levels and a decline in glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) activity, was significantly alleviated by fibrauretine pretreatment. The suppression of the neuroinflammatory response by fibrauretine was realized not only by the decrease in the levels of tumour necrosis factor- (TNF-) and interleukin-1 (IL-1) in the brain tissues and by the enzyme-linked immunosorbent assay (ELISA) but also by the protein expression levels of nuclear factor-B (NF-B), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), which were measured by immunohistochemistry and western blotting. In addition, the protein expression levels of inflammatory factors interleukin-33 (IL-33) and ST2 in the brain tissues were detected by immunohistochemistry. Furthermore, the effects of western blotting demonstrated that the administration of fibrauretine significantly suppressed the protein expression levels of caspase-3, cleaved caspase-3, and Bax and increased the protein expression levels of Bcl-2, and the results of the H&E and TUNEL assay all suggested the inhibition of apoptosis in the neurons. The results clearly suggest that the underlying molecular mechanisms of action of the fibrauretine-mediated alleviation of d-galactose/AlCl3-induced Alzheimer's disease may involve antioxidant, anti-inflammatory, and anti-apoptotic effects.
机译：Fibrauretine是Fibraurea recisa皮尔从藤的主要活性成分之一茎它具有一系列显著药理作用。目的是评价在所述潜在的抗阿尔茨海默氏病（AD）fibrauretine的影响本研究d半乳糖/三氯化铝诱导的小鼠模型中，与行动的底层机制进一步研究首次。我们的研究结果显示，与fibrauretine该预处理显著改善了模型小鼠的空间短期工作记忆的Y型迷宫测试中的能力，以及空间学习和记忆的Morris水迷宫中的能力。脑组织的淀粉样蛋白（A），P-头，头和乙酰胆碱酯酶的水平d半乳糖/三氯化铝酣小鼠显着增加，并且这些作用被fibrauretine逆转。相反，在神经递质乙酰胆碱（ACh）和的电平的增加显著胆碱乙酰转移酶（ChAT的）在fibrauretine处理组中观察到与模型组相比。神经元的氧化应激，通过增加的丙二醛（MDA）和一氧化氮（NO）水平和谷胱甘肽（GSH）的下降，过氧化氢酶（CAT）和超氧化物歧化酶（SOD）活性所证明，通过fibrauretine预处理显著减轻。通过fibrauretine所述神经炎性响应的抑制不仅通过在脑组织中肿瘤坏死因子（TNF-α）和白细胞介素-1（IL-1）的水平的降低，并通过酶联免疫吸附测定（ELISA实现），而且还通过核因子（NF-B）的蛋白质表达水平，环氧合酶-2（COX-2），和诱导型一氧化氮合酶（iNOS），这是由免疫组织化学和蛋白印迹测定。此外，通过免疫组织化学检测到的炎症因子白细胞介素33（IL-33）和ST2在脑组织中的蛋白质表达水平。此外，蛋白质印迹的效果表明，fibrauretine施用显著抑制胱天蛋白酶-3，裂解的caspase-3，和Bax的蛋白表达水平，增加的Bcl-2蛋白表达水平，和H＆E和TUNEL的结果测定所有建议的细胞凋亡的神经元的抑制。结果清楚地表明，d半乳糖/三氯化铝诱导的阿耳茨海默氏病的fibrauretine介导的减轻作用的潜在分子机制可能涉及抗氧化，抗炎和抗细胞凋亡作用。

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  • 来源
    《RSC Advances》 |2018年第55期|共12页
  • 作者

    Xing Zhiheng; He Zhongmei; Wang Shuning; Yan Yu; Zhu Hongyan; Gao Yugang; Zhao Yan; Zhang Lianxue;

  • 作者单位

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

    Jilin Agr Univ Changchun 130118 Jilin Peoples R China;

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