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诸如[具体物质1]和[具体物质2]之类的天然化合物可调节小鼠鱼藤酮诱导的帕金森病中的神经炎症、氧化应激和脂氧素A4表达。

Natural Compounds Such as and Modulate Neuroinflammation, Oxidative Stress and Lipoxin A4 Expression in Rotenone-Induced Parkinson's Disease in Mice.

作者信息

Cordaro Marika, Modafferi Sergio, D'Amico Ramona, Fusco Roberta, Genovese Tiziana, Peritore Alessio Filippo, Gugliandolo Enrico, Crupi Rosalia, Interdonato Livia, Di Paola Davide, Impellizzeri Daniela, Cuzzocrea Salvatore, Calabrese Vittorio, Di Paola Rosanna, Siracusa Rosalba

机构信息

Department of Biomedical, Dental and Morphological and Functional Imaging, University of Messina, 98125 Messina, Italy.

Department of Biomedical and Biotechnological Sciences, University of Catania, 95125 Catania, Italy.

出版信息

Biomedicines. 2022 Oct 7;10(10):2505. doi: 10.3390/biomedicines10102505.

DOI:10.3390/biomedicines10102505
PMID:36289766
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9599271/
Abstract

BACKGROUND

A growing body of research suggests that oxidative stress and neuroinflammation are early pathogenic features of neurodegenerative disorders. In recent years, the vitagene system has emerged as a potential target, as it has been shown to have a high neuroprotective power. Therefore, the discovery of molecules capable of activating this system may represent a new therapeutic target to limit the deleterious consequences induced by oxidative stress and neuroinflammation, such as neurodegeneration. Lipoxins are derived from arachidonic acid, and their role in the resolution of systemic inflammation is well established; however, they have become increasingly involved in the regulation of neuroinflammatory and neurodegenerative processes. Our study aimed at activating the NF-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) redox system and increasing lipoxin A4 for the modulation of antioxidant stress and neuroinflammation through the action of two fungi in a rotenone-induced Parkinson's model.

METHODS

During the experiment, mice received , or a combination of the two (200 mg/kg, orally) concomitantly with rotenone (5 mg/kg, orally) for 28 days.

RESULTS

The results obtained highlighted the ability of these two fungi and, in particular, their ability through their association to act on neuroinflammation through the nuclear factor-kB pathway and on oxidative stress through the Nrf2 pathway. This prevented dopaminergic neurons from undergoing apoptosis and prevented the alteration of typical Parkinson's disease (PD) markers and α-synuclein accumulation. The action of and was also able to limit the motor and non-motor alterations characteristic of PD.

CONCLUSIONS

Since these two mushrooms are subject to fewer regulations than traditional drugs, they could represent a promising nutraceutical choice for preventing PD.

摘要

背景

越来越多的研究表明,氧化应激和神经炎症是神经退行性疾病的早期致病特征。近年来,维生素基因系统已成为一个潜在靶点,因为它已被证明具有很高的神经保护能力。因此,发现能够激活该系统的分子可能代表一个新的治疗靶点,以限制氧化应激和神经炎症诱导的有害后果,如神经退行性变。脂氧素衍生自花生四烯酸,它们在全身炎症消退中的作用已得到充分证实;然而,它们越来越多地参与神经炎症和神经退行性过程的调节。我们的研究旨在通过两种真菌在鱼藤酮诱导的帕金森病模型中的作用,激活核因子E2相关因子2(Nrf2)/血红素加氧酶1(HO-1)氧化还原系统并增加脂氧素A4,以调节抗氧化应激和神经炎症。

方法

在实验过程中,小鼠接受、或两者的组合(200mg/kg,口服),同时给予鱼藤酮(5mg/kg,口服),持续28天。

结果

获得的结果突出了这两种真菌的能力,特别是它们通过联合作用通过核因子-κB途径作用于神经炎症,并通过Nrf2途径作用于氧化应激的能力。这防止了多巴胺能神经元发生凋亡,并防止了典型帕金森病(PD)标志物的改变和α-突触核蛋白的积累。和的作用还能够限制PD特有的运动和非运动改变。

结论

由于这两种蘑菇比传统药物受到的监管更少,它们可能是预防PD的一种有前途的营养保健品选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/085ebc63fc14/biomedicines-10-02505-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/fe38b37f0592/biomedicines-10-02505-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/831ed63d9d9c/biomedicines-10-02505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/37e01bc1bd25/biomedicines-10-02505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/5fd850dce96b/biomedicines-10-02505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/110b80df04a3/biomedicines-10-02505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/945d2fff348d/biomedicines-10-02505-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/085ebc63fc14/biomedicines-10-02505-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/fe38b37f0592/biomedicines-10-02505-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/ac93502672cc/biomedicines-10-02505-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/831ed63d9d9c/biomedicines-10-02505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/37e01bc1bd25/biomedicines-10-02505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/5fd850dce96b/biomedicines-10-02505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/110b80df04a3/biomedicines-10-02505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/945d2fff348d/biomedicines-10-02505-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e08/9599271/085ebc63fc14/biomedicines-10-02505-g008.jpg

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