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α-生育酚可保护脂多糖激活的 BV2 小胶质细胞。

α-Tocopherol Protects Lipopolysaccharide-Activated BV2 Microglia.

机构信息

Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.

Department of Biosciences, Biotechnologies and Environment, University of Bari, 70125 Bari, Italy.

出版信息

Molecules. 2023 Apr 10;28(8):3340. doi: 10.3390/molecules28083340.

Abstract

Microglia, the resident macrophage-like population in the central nervous system, play a crucial role in the pathogenesis of many neurodegenerative disorders by triggering an inflammatory response that leads to neuronal death. Neuroprotective compounds to treat or prevent neurodegenerative diseases are a new field of study in modern medicine. Microglia are activated in response to inflammatory stimuli. The pathogenesis of various neurodegenerative diseases is closely related to the constant activation of microglia due to their fundamental role as a mediator of inflammation in the brain environment. α-Tocopherol, also known as vitamin E, is reported to possess potent neuroprotective effects. The goal of this study was to investigate the biological effects of vitamin E on BV2 microglial cells, as a possible neuroprotective and anti-inflammatory agent, following stimulation with lipopolysaccharide (LPS). The results showed that the pre-incubation of microglia with α-tocopherol can guarantee neuroprotective effects during microglial activation induced by LPS. α-Tocopherol preserved the branched morphology typical of microglia in a physiological state. It also reduced the migratory capacity; the production of pro-inflammatory and anti-inflammatory cytokines such as TNF-α and IL-10; and the activation of receptors such as TRL4 and CD40, which modulate the PI3K-Akt signaling pathway. The results of this study require further insights and research, but they present new scenarios for the application of vitamin E as an antioxidant for the purpose of greater neuroprotection in vivo for the prevention of possible neurodegenerative diseases.

摘要

小胶质细胞是中枢神经系统中固有样巨噬细胞群体,通过触发炎症反应导致神经元死亡,在许多神经退行性疾病的发病机制中发挥关键作用。神经保护化合物是治疗或预防神经退行性疾病的现代医学的一个新研究领域。小胶质细胞对炎症刺激作出反应而被激活。各种神经退行性疾病的发病机制与小胶质细胞的持续激活密切相关,因为它们是大脑环境中炎症的主要介质。α-生育酚,也称为维生素 E,据报道具有很强的神经保护作用。本研究旨在研究维生素 E 对脂多糖(LPS)刺激的 BV2 小胶质细胞的生物学作用,作为一种可能的神经保护和抗炎剂。结果表明,α-生育酚预先孵育小胶质细胞可以保证 LPS 诱导的小胶质细胞激活期间的神经保护作用。α-生育酚保留了小胶质细胞在生理状态下的分支形态。它还降低了迁移能力;产生促炎和抗炎细胞因子,如 TNF-α和 IL-10;以及激活调节 PI3K-Akt 信号通路的受体,如 TRL4 和 CD40。本研究的结果需要进一步的见解和研究,但它们为维生素 E 作为抗氧化剂的应用提供了新的场景,目的是在体内实现更大的神经保护,预防可能的神经退行性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/095e/10141518/72470ae0a682/molecules-28-03340-g001.jpg

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