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Coconut Oil Alleviates the Oxidative Stress-Mediated Inflammatory Response via Regulating the MAPK Pathway in
Xinyu Chen1,2, Dong Im Kim1, Hi-Gyu Moon1
1Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-gil, Jeongeup-si 56212, Korea.
Abstract:
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.
Insights
Coconut oil reduces inflammation caused by particulate matter (PM) exposure in alveolar macrophages (AMs). It mitigates oxidative stress and cytokine production by regulating the toll-like receptor 4/mitogen-activated protein kinase pathway.
Area of Science:
- Immunology
- Environmental Health
- Toxicology
- Nutritional Science
Background:
- Particulate matter (PM) exposure is linked to respiratory diseases, impacting the respiratory immune system.
- Alveolar macrophages (AMs) are crucial in respiratory inflammation, mediating immune responses to pathogens and pollutants.
- Coconut oil possesses known antioxidant and anti-inflammatory properties, but its protective effects against PM-induced respiratory inflammation in AMs are underexplored.
Purpose of the Study:
- To investigate the protective effects of coconut oil against artificial PM (APM) and diesel exhaust particles (DEP)-induced cytotoxicity and inflammation in AMs.
- To elucidate the underlying molecular mechanisms, including oxidative stress, cytokine production, and signaling pathways involved in PM-induced AM responses.
- To evaluate coconut oil's potential to mitigate PM-induced respiratory immune system damage.
Main Methods:
- Generated artificial PM (APM) with a ~30 nm diameter and compared its cytotoxicity with diesel exhaust particles (DEP).
- Stimulated AMs with APM and DEP, then assessed cell viability, oxidative stress markers (ROS, GSSG/GSH ratio), and cytokine production (TNF-α, IL-1β, IL-6).
- Analyzed the expression of genes (CXCL1, MCP-1) and proteins (TLR4, MAPK pathway components) involved in inflammatory signaling.
Main Results:
- APM and DEP exhibited significant dose-dependent cytotoxicity in AMs, decreasing cell viability and increasing oxidative stress markers.
- PM exposure upregulated pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), chemokines (CXCL1, MCP-1), and key signaling proteins (TLR4, MAPK pathway).
- Coconut oil treatment reversed these detrimental effects, reducing cytotoxicity, oxidative stress, and inflammation markers in PM-exposed AMs.
Conclusions:
- Coconut oil demonstrates significant protective effects against APM- and DEP-induced inflammation and oxidative stress in alveolar macrophages.
- These protective effects are mediated through the regulation of the toll-like receptor 4 (TLR4)/mitogen-activated protein kinase (MAPK) signaling pathway.
- Coconut oil holds potential as a dietary intervention to mitigate adverse respiratory health effects associated with particulate matter exposure.
