Department of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea.
Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea.
BMB Rep. 2017 Dec;50(12):634-639. doi: 10.5483/bmbrep.2017.50.12.189.
We aimed to assess the anti-inflammatory and antioxidative properties of KHG26792, a novel azetidine derivative, in amyloid β (Aβ)-treated primary microglial cells. KHG26792 attenuated the Aβ-induced production of inflammatory mediators such as IL-6, IL-1β, TNF-α, and nitric oxide. The levels of protein oxidation, lipid peroxidation, ROS, and NADHP oxidase enhanced by Aβ were also downregulated by KHG26792 treatment. The effects of KHG26792 against the Aβ-induced increases in inflammatory cytokine levels and oxidative stress were achieved by increasing the phosphorylation of Akt/ GSK-3β signaling and by decreasing the Aβ-induced translocation of NF-κB. Our results provide novel insights into the use of KHG26792 as a potential agent against Aβ toxicity, including its role in the reduction of inflammation and oxidative stress. Nevertheless, further investigations of cellular signaling are required to clarify the in vivo effects of KHG26792 against Aβ-induced toxicity. [BMB Reports 2017; 50(12): 634-639].
我们旨在评估新型氮杂环丁烷衍生物 KHG26792 在淀粉样β（Aβ）处理的原代小胶质细胞中的抗炎和抗氧化特性。KHG26792 减弱了 Aβ 诱导的炎症介质（如 IL-6、IL-1β、TNF-α 和一氧化氮）的产生。Aβ 增强的蛋白质氧化、脂质过氧化、ROS 和 NADHP 氧化酶水平也被 KHG26792 处理下调。通过增加 Akt/GSK-3β 信号的磷酸化和减少 Aβ 诱导的 NF-κB 易位，KHG26792 对 Aβ 诱导的炎症细胞因子水平和氧化应激增加的作用得以实现。我们的结果为将 KHG26792 用作对抗 Aβ 毒性的潜在药物提供了新的见解，包括其在减轻炎症和氧化应激方面的作用。然而，需要进一步研究细胞信号转导，以阐明 KHG26792 对 Aβ 诱导的毒性的体内作用。[BMB 报告 2017；50(12):634-639]。
