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白藜芦醇对β-甲基氨基丙氨酸诱导的星形胶质细胞功能障碍的神经保护作用。

Glioprotective Effects of Resveratrol Against BMAA-Induced Astroglial Dysfunctions.

作者信息

Dias Filipe Renato Pereira, de Souza Almeida Rômulo Rodrigo, Sovrani Vanessa, Thomaz Natalie K, Gonçalves Carlos-Alberto, Quincozes-Santos André, Bobermin Larissa Daniele

机构信息

Programa de Pós-Graduação Em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rua Ramiro Barcelos, 2600 - Anexo, 90035-003, RS, Brazil.

Programa de Pós-Graduação Em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

出版信息

Neurotox Res. 2022 Apr;40(2):530-541. doi: 10.1007/s12640-022-00492-9. Epub 2022 Mar 23.

Abstract

Astroglial cells play important roles in maintaining central nervous system (CNS) homeostasis. The neurotoxin β-N-methylamino-L-alanine (BMAA) has usually been associated with neurodegeneration due to its toxic effects on neurons. However, little is known about the effects of BMAA on astroglial cells. Resveratrol, a natural polyphenol, represents a potential protective strategy against brain injuries. In the present study, we sought to investigate BMAA-induced astroglial dysfunctions and the glioprotective roles of resveratrol. BMAA did not impair astroglial cellular viability, but increased glutamate uptake, glutamate metabolism into glutamine, and reactive oxygen species production, while decreased glutathione (GSH) and superoxide dismutase (SOD)-based antioxidant defenses and triggers an inflammatory response. In contrast, resveratrol was able to prevent most of these BMAA-induced functional changes in astroglial cells. Moreover, both BMAA and resveratrol modulated the gene expression of molecular pathways associated with glutamate metabolism, redox homeostasis, and inflammatory response, which characterize their roles on astroglial functions. In this regard, BMAA downregulated adenosine receptors, peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α), phosphoinositide-3-kinase (PI3K), and Akt, while resveratrol prevented these effects and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Our study, for the first time, demonstrates that BMAA directly impacts key astroglial functions, contributing to elucidating the cellular and molecular mechanisms of this toxin in the CNS. In addition, we reinforce the glioprotective effects of resveratrol against BMAA-induced astroglial dysfunctions.

摘要

星形胶质细胞在维持中枢神经系统(CNS)稳态中发挥着重要作用。神经毒素β-N-甲基氨基-L-丙氨酸(BMAA)通常因其对神经元的毒性作用而与神经退行性变相关。然而,关于BMAA对星形胶质细胞的影响知之甚少。白藜芦醇是一种天然多酚,是对抗脑损伤的一种潜在保护策略。在本研究中,我们试图探究BMAA诱导的星形胶质细胞功能障碍以及白藜芦醇的神经胶质保护作用。BMAA并未损害星形胶质细胞的活力,但增加了谷氨酸摄取、谷氨酸代谢为谷氨酰胺以及活性氧的产生,同时降低了基于谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的抗氧化防御,并引发了炎症反应。相比之下,白藜芦醇能够预防BMAA诱导的星形胶质细胞的大多数这些功能变化。此外,BMAA和白藜芦醇都调节了与谷氨酸代谢、氧化还原稳态和炎症反应相关的分子途径的基因表达,这表征了它们在星形胶质细胞功能中的作用。在这方面,BMAA下调了腺苷受体、过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1α)、磷脂酰肌醇-3-激酶(PI3K)和Akt,而白藜芦醇则预防了这些作用并上调了核因子红细胞2相关因子2(Nrf2)和血红素加氧酶-1(HO-1)。我们的研究首次表明,BMAA直接影响关键的星形胶质细胞功能,有助于阐明这种毒素在中枢神经系统中的细胞和分子机制。此外,我们强化了白藜芦醇对BMAA诱导的星形胶质细胞功能障碍的神经胶质保护作用。

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