Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-gil, Jeongeup-si 56212, Korea.
Department of Human and Environmental Toxicology, University of Science & Technology, Daejeon 34113, Korea.
Molecules. 2022 May 2;27(9):2898. doi: 10.3390/molecules27092898.
Exposure to particulate matter (PM) is related to various respiratory diseases, and this affects the respiratory immune system. Alveolar macrophages (AMs), which are defenders against pathogens, play a key role in respiratory inflammation through cytokine production and cellular interactions. Coconut oil demonstrates antioxidant and anti-inflammatory properties, and it is consumed worldwide for improved health. However, reports on the protective effects of coconut oil on the PM-induced respiratory immune system, especially in AMs, are limited. In this study, we generated artificial PM (APM) with a diameter approximately of 30 nm by controlling the temperature, and compared its cytotoxicity with diesel exhaust particles (DEP). We also investigated the antioxidant and anti-inflammatory effects of coconut oil in APM− and DEP−stimulated AMs, and the underlying molecular mechanisms. Our results showed that APM and DEP had high cytotoxicity in a dose-dependent manner in AMs. In particular, APM or DEP at 100 μg/mL significantly decreased cell viability (p < 0.05) and significantly increased oxidative stress markers such as reactive oxygen species (p < 0.01); the GSSH/GSH ratio (p < 0.01); and cytokine production, such as tumor necrosis factor-α (p < 0.001), interleukin (IL)-1β (p < 0.001), and IL-6 (p < 0.001). The expression of the genes for chemokine (C-X-C motif) ligand-1 (p < 0.05) and monocyte chemoattractant protein-1 (p < 0.001); and the proteins toll-like receptor (TLR) 4 (p < 0.01), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (p < 0.001), p38 (p < 0.001); and extracellular receptor-activated kinase (p < 0.001), were also upregulated by PM. These parameters were reversed upon treatment with coconut oil in APM− or DEP−stimulated AMs. In conclusion, coconut oil can reduce APM− or DEP−induced inflammation by regulating the TLR4/MAPK pathway in AMs, and it may protect against adverse respiratory effects caused by PM exposure.
颗粒物 (PM) 暴露与各种呼吸道疾病有关，这会影响呼吸道免疫系统。肺泡巨噬细胞 (AMs) 作为病原体的防御者，通过细胞因子的产生和细胞间相互作用在呼吸炎症中发挥关键作用。椰子油具有抗氧化和抗炎特性，它在全球范围内被消费以改善健康。然而，关于椰子油对 PM 诱导的呼吸道免疫系统的保护作用的报告，尤其是在 AMs 中，是有限的。在这项研究中，我们通过控制温度生成了直径约为 30nm 的人工 PM (APM)，并将其细胞毒性与柴油 exhaust particles (DEP) 进行了比较。我们还研究了椰子油在 APM 和 DEP 刺激的 AMs 中的抗氧化和抗炎作用，以及潜在的分子机制。我们的结果表明，APM 和 DEP 在 AMs 中呈剂量依赖性具有高细胞毒性。特别是，APM 或 DEP 在 100μg/mL 时显著降低细胞活力 (p < 0.05)，并显著增加氧化应激标志物，如活性氧 (p < 0.01)；GSSH/GSH 比 (p < 0.01)；和细胞因子产生，如肿瘤坏死因子-α (p < 0.001)、白细胞介素 (IL)-1β (p < 0.001) 和 IL-6 (p < 0.001)。趋化因子 (C-X-C 基序) 配体-1 (p < 0.05) 和单核细胞趋化蛋白-1 (p < 0.001) 的基因表达；以及 toll-like receptor (TLR) 4 (p < 0.01)、丝裂原激活蛋白激酶 (MAPK) 和 c-Jun N-terminal kinase (p < 0.001)、p38 (p < 0.001)；和细胞外受体激活激酶 (p < 0.001) 的蛋白质也被 PM 上调。在用椰子油处理 APM 或 DEP 刺激的 AMs 后，这些参数得到了逆转。总之，椰子油可以通过调节 AMs 中的 TLR4/MAPK 通路来减少 APM 或 DEP 引起的炎症，并且它可能可以防止 PM 暴露引起的不良呼吸道影响。
