Sargassum horneri (Turner) inhibit urban particulate matter-induced inflammation in MH-S lung macrophages via blocking TLRs mediated NF-kappa B and MAPK activation

Ethnopharmacological relevance: Sargassum horneri is a nutrient rich edible brown seaweed with numerous biological properties found in shallow coastal areas of Korean peninsula. S. horned traditionally used as a medicinal ingredient to treat several disease conditions such as hyperlipidemia, hypertension, heart disease, and inflammatory diseases (furuncle). However, to utilize S. horneri as an active ingredient for functional foods and human health applications requires to conform the bioactive properties and underlying mechanisms of those activities. Aim of the study: Here, we investigated anti-inflammatory mechanisms of commercial grade 70% ethanol extract separated from S. horneri (SHE) on inflammatory response in particulate matter (PM)-induced MH-S lung macrophages; where PM in breathable air one of the major health concern in Korea. Materials and methods: We compared the anti-inflammatory effects of SHE on the activity of toll-like receptors (TLR) activation, NF-kappa B, MAPKs, and pro-inflammatory cytokine secretion in MH-S lung macrophages exposed to PM as a lung inflammation model. Results: According to the results, PM-stimulation, induced the levels of NO, PGE2, TNF-alpha, IL-1 beta, IL-6, iNOS, and COX2 (P < 0.05) in MH-S macrophages. In addition, phosphorylation levels of NF-kappa B and MAPKs were also increased with the PM stimulation through the upregulated expression of TLR. However, SHE treatment significantly repressed the secretions of inflammatory cytokines and reduced protein expression such as PGE2, TNF-alpha, IL-6, IL-1 beta, NF-kappa B, and MAPKs from PM-activated macrophages. Specifically, SHE inhibited the upregulated mRNA expression levels of TLR2, TLR3, TLR4, and TLR7 in PM-induced MH-S cells; known biomarkers of downstream activation of NF-kappa B and MAPKs. Conclusion: These results suggested that SHE is a potential inhibitor of PM-induced inflammatory responses in lung macrophages. Thus, SHE could inhibit PM-induced chronic inflammation in lungs via blocking TLR/NF-kappa B/MAPKs signal transduction. Therefore, it was concluded that SHE may be a useful substance to develop as functional product to reduce inflammation against PM-induced inflammation.