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香草醛通过调节 LPS 刺激的小胶质细胞中的炎症因子和 NF-κB 信号通路发挥抗神经炎症作用。

Anti-Neuroinflammatory Effects of Vanillin Through the Regulation of Inflammatory Factors and NF-κB Signaling in LPS-Stimulated Microglia.

机构信息

Department of Life Science, Immunology Research Lab, BK21-plus Research Team for Bioactive Control Technology, College of Natural Sciences, Chosun University, Dong-gu, Gwangju, 501-759, Republic of Korea.

Djkunghee Hospital, Department of Preventive and Society Dentistry, School of Dentistry, Kyung Hee University, Seoul, 02447, South Korea.

出版信息

Appl Biochem Biotechnol. 2019 Mar;187(3):884-893. doi: 10.1007/s12010-018-2857-5. Epub 2018 Aug 10.

Abstract

Microglia, resident macrophages of the central nervous system (CNS), is responsible for immune responses and homeostasis of the CNS. Microglia plays a complex role in neuroinflammation, which has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Therefore, therapeutic agents that suppress the microglia-mediated inflammatory response could potentially be used in the prevention or treatment of neurodegenerative diseases. Vanillin, a primary component of vanilla bean extract, has anti-inflammatory, anticancer, and antitumor properties. However, the effects of vanillin on the anti-neuroinflammatory responses of microglial cells are still poorly understood. In this study, we investigated the mechanism by which vanillin induces anti-neuroinflammatory responses in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. We found that vanillin significantly decreased the production of nitric oxide and pro-inflammatory cytokines, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Vanillin also reduced the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the mRNA expression levels of IL-1β, TNF-α, and IL-6. Moreover, vanillin inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB. Collectively, these results suggest that vanillin has anti-neuroinflammatory properties and may act as a natural therapeutic agent for neuroinflammatory diseases.

摘要

小胶质细胞是中枢神经系统 (CNS) 的固有巨噬细胞,负责 CNS 的免疫反应和稳态。小胶质细胞在神经炎症中发挥着复杂的作用,神经炎症与阿尔茨海默病和帕金森病等神经退行性疾病有关。因此,抑制小胶质细胞介导的炎症反应的治疗剂可能可用于预防或治疗神经退行性疾病。香草醛是香草豆提取物的主要成分,具有抗炎、抗癌和抗肿瘤特性。然而,香草醛对小胶质细胞的抗神经炎症反应的影响仍知之甚少。在这项研究中,我们研究了香草醛在脂多糖 (LPS) 刺激的 BV-2 小胶质细胞中诱导抗神经炎症反应的机制。我们发现香草醛可显著降低一氧化氮和促炎细胞因子(包括白细胞介素 (IL)-1β、肿瘤坏死因子-α (TNF-α) 和白细胞介素-6 (IL-6))的产生。香草醛还降低了诱导型一氧化氮合酶 (iNOS) 和环氧化酶-2 (COX-2) 的蛋白水平,以及 IL-1β、TNF-α 和 IL-6 的 mRNA 表达水平。此外,香草醛抑制丝裂原活化蛋白激酶 (MAPKs) 和核因子 (NF)-κB 的磷酸化。总之,这些结果表明香草醛具有抗神经炎症特性,可能是神经炎症性疾病的天然治疗剂。

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