Abstract
Ethnopharmacological relevanceSargassum horneri (Turner) C. Agardh (S. horneri), an edible brown marine algae, is known to have immunomodulatory effects and has been used in oriental medicine to treat inflammatory diseases. It is well known that ambient particulate matter (PM) is closely related to increased respiratory diseases inducing lung inflammation. AimConsidering the use of Sargassum horneri in traditional medicine to treat inflammatory diseases, we hypothesized and investigated the use of Sargassum horneri containing polyphenols against PM-induced inflammatory responses. Materials and methodsIn this study, we evaluated the impact of PM (majority <2.5 μm in diameter) on deep bronchial penetration ability upon inhalation and a therapeutic approach to mitigate its harmful effects using an ethanol extract of Sargassum horneri, an edible brown algae, containing polyphenols on a type II alveolar epithelial cell line, MLE-12. ResultsPM triggered mRNA expression of toll-like receptors (TLRs) TLR2/4/7, and those TLRs were significantly attenuated by Sargassum horneri extract (SHE). SHE further attenuated the phosphorylation of mitogen-activated protein kinase (MAPK) p38, extracellular signal-regulated kinase 1/2 (Erk1/2), and c-Jun NH (2)-terminal kinase (JNK), which were also activated in PM-exposed cells. Altogether, SHE subdued the PM-induced mRNA expression of pro-inflammatory cytokines (interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6) and lung epithelial cell derived-chemokines (IL-8, monocyte chemoattractant protein-1 (MCP-1), and chemokine (C–C motif) ligand 5 (CCL5)). SHE also suppressed the mRNA expression of PM-induced pro-allergic cytokines thymic stromal lymphopoietin (TSLP) and interleukin (IL)-33. Furthermore, we showed that SHE suppressed the MAPK-dependent signaling pathway by attenuating receptor-associated factor (TRAF) 6 activation of proteins MyD88 and TNF. ConclusionTaking all the data together, we suggest that the anti-inflammatory potential of SHE on PM-exposed MLE-12 cells is mediated by the inhibition of PM-triggered downstream signaling along the TLR2/4/7–MyD88–TRAF6 axis of MAPK signaling.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.