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毒死蜱农药促进 BV-2 小胶质细胞氧化应激和炎症状态:在神经炎症中的作用。

Chlorpyrifos pesticide promotes oxidative stress and increases inflammatory states in BV-2 microglial cells: A role in neuroinflammation.

机构信息

Department of Food Science and Technology, Federal University of Santa Maria, Santa Maria, RS, Brazil.

Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.

出版信息

Chemosphere. 2021 Sep;278:130417. doi: 10.1016/j.chemosphere.2021.130417. Epub 2021 Mar 29.

DOI:10.1016/j.chemosphere.2021.130417
PMID:33839396
Abstract

The exposure to environmental stressors, such as organophosphate (OP) pesticides, has been associated with the development of neurodegenerative diseases. Chlorpyrifos (CPF) is the worldwide most used OP pesticide and one of the most hazardous pesticides as it can cross the blood-brain barrier. Since studies evaluating the effects of CPF on brain immune cells are scarce, this research investigated the oxidative and inflammatory responses of CPF exposure in murine microglial cells. BV-2 cells were exposed to different concentrations of CPF pesticide (0.3-300 μM). CPF induced activation of microglial cells, confirmed by Iba-1 and CD11b marking, and promoted microglial proliferation and cell cycle arrest at S phase. Moreover, CPF exposure increased oxidative stress production (NO, MDA, and O∙), and upregulated pro-inflammatory cytokines (IL-1β and NLRP3) genes expression in BV-2 cells. Overall, data showed that CPF exposure, at the lowest concentrations, acted by promoting pro-oxidative and pro-inflammatory states in microglial cells. These results provide important information on the potential role of microglial activation in CPF-induced neuroinflammation and add to the expanding knowledge on the neurotoxicity of OP.

摘要

暴露于环境应激物,如有机磷(OP)农药,与神经退行性疾病的发展有关。毒死蜱(CPF)是世界上使用最广泛的 OP 农药之一,也是最危险的农药之一,因为它可以穿过血脑屏障。由于评估 CPF 对大脑免疫细胞影响的研究较少,因此本研究调查了 CPF 暴露对小鼠小胶质细胞的氧化和炎症反应。BV-2 细胞暴露于不同浓度的 CPF 农药(0.3-300 μM)。CPF 通过 Iba-1 和 CD11b 标记物激活小胶质细胞,并促进小胶质细胞增殖和细胞周期停滞在 S 期。此外,CPF 暴露增加了氧化应激产物(NO、MDA 和 O∙)的产生,并上调了 BV-2 细胞中促炎细胞因子(IL-1β 和 NLRP3)基因的表达。总的来说,数据表明 CPF 暴露在最低浓度下通过促进小胶质细胞中的促氧化和促炎状态发挥作用。这些结果提供了有关小胶质细胞激活在 CPF 诱导的神经炎症中的潜在作用的重要信息,并为 OP 的神经毒性知识的扩展做出了贡献。

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