Coconut Oil Alleviates the Oxidative Stress-Mediated Inflammatory Response via Regulating the MAPK Pathway in Particulate Matter-Stimulated Alveolar Macrophages.

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.