Department of Food and Biotechnology, Korea University, Sejong 30019, Republic of Korea.
BK21 FOUR Research Group for Omics-Based Bio-Health in Food Industry, Korea University, Sejong 30019, Republic of Korea.
Int J Mol Sci. 2023 Jan 17;24(3):1858. doi: 10.3390/ijms24031858.
The direct effects of particulate matter (PM) on lung injury and its specific molecular mechanisms are unclear. However, experimental evidence has shown that oxidative stress-mediated inflammation in macrophages is the main pathological outcome of PM exposure. Curcumin has been reported to protect organs against the disturbance of homeostasis caused by various toxic agents through anti-inflammatory and antioxidative effects. However, the protective action of curcumin against PM-induced pulmonary inflammation and the underlying mechanism have not been thoroughly investigated. In this study, we established a PM-induced pulmonary inflammation mouse model using the intratracheal instillation method to investigate the protective ability of curcumin against PM-induced pulmonary inflammation. Compared to the mice treated with PM only, the curcumin-treated mice showed alleviated alveolar damage, decreased immune cell infiltration, and reduced proinflammatory cytokine production in both lung tissue and BALF. To evaluate the underlying mechanism, the mouse macrophage cell line RAW264.7 was used. Pretreatment with curcumin prevented the production of PM-induced proinflammatory cytokines by deactivating NF-κB through the suppression of MAPK signaling pathways. Furthermore, curcumin appears to attenuate PM-induced oxidative stress through the activation of Nrf2 and downstream antioxidant signaling. Our findings demonstrate that curcumin protects against PM-induced lung injury by suppressing oxidative stress and inflammatory activation in macrophages.
颗粒物 (PM) 对肺部损伤的直接影响及其特定的分子机制尚不清楚。然而,实验证据表明,氧化应激介导的巨噬细胞炎症是 PM 暴露的主要病理结果。姜黄素已被报道通过抗炎和抗氧化作用来保护器官免受各种毒性物质引起的内稳态紊乱。然而,姜黄素对 PM 诱导的肺部炎症的保护作用及其潜在机制尚未得到深入研究。在这项研究中,我们使用气管内滴注法建立了 PM 诱导的肺部炎症小鼠模型,以研究姜黄素对 PM 诱导的肺部炎症的保护作用。与仅用 PM 处理的小鼠相比,姜黄素处理的小鼠显示出肺泡损伤减轻、免疫细胞浸润减少以及肺组织和 BALF 中促炎细胞因子产生减少。为了评估潜在的机制,我们使用了小鼠巨噬细胞系 RAW264.7。姜黄素预处理通过抑制 MAPK 信号通路使 NF-κB 失活,从而防止 PM 诱导的促炎细胞因子的产生。此外,姜黄素似乎通过激活 Nrf2 和下游抗氧化信号来减轻 PM 诱导的氧化应激。我们的研究结果表明,姜黄素通过抑制巨噬细胞中的氧化应激和炎症激活来防止 PM 诱导的肺损伤。