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. 2022 May 2;27(9):2898. doi: 10.3390/molecules27092898

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Effects of coconut oil on oxidative stress in artificial particulate matter (APM) and diesel exhaust particles (DEP)−stimulated alveolar macrophages (MH−S). (A,B) Cytotoxicity assessment of distilled water (DW) and coconut oil the 3–(4,5–dimethylthiazol–2–yl)–2,5–diphenyltetrazolium bromide (MTT) assay. (C) Cytotoxicity assessment of coconut oil in APM and DEP−stimulated MH−S. (D) Reactive oxygen species (ROS) production was measured using 2′,7′−dichlorofluorescein diacetate (DCF−DA) staining. Data represent the mean ± SD (n = 8 per group). (E) NADPH dehydrogenase (quinone) (NQO1) gene level was measured using real−time PCR. (F) Glutathione (GSH), (G) glutathione disulfide (GSSG), (H) GSSG/GSH ratio, and (I) Nicotinamide adenine dinucleotide phosphate (NADPH) levels in MH−S. Negative controls (NC) are untreated samples. Vehicle control (VC) was treated with cell medium including 10% DW. Data are presented as the means ± SD of three independent experiments. * p < 0.05, ** p < 0.01 or *** p < 0.001, **** p < 0.0001 vs. NC or VC; ^## p < 0.01 or ^### p < 0.001 vs. APM group; ^§§ p < 0.01 or ^§§§ p < 0.001 vs. DEP group.