원문정보
초록
영어
Air pollution is a process that mixes pollutants into the atmosphere, which is potentially harmful to humans and causes negative impacts on the surrounding environment (biotic and abiotic). The negative health effects associated with air pollution have been reported from both indoor and outdoor environments. Specifically, dust storms originating in Chinese and Mongolian desert areas introduce significant amounts of particulate matter (PM) to the Korean atmosphere. Previously, several studies reported that urban PM (UPM) is a potential agent that causes inflammation in the lungs by altering multiple signal transduction pathways; therefore, screening and identification of anti-inflammatory compounds against UPM-induced inflammation is an urgent requirement. In the present study, we attempted to study the anti-inflammatory properties of 3-Hydroxy-5,6-epoxy-β- ionone (HEBI), a pure compound isolated from invasive brown seaweed, Sargassum horneri (brown edible seaweed), against UPM-stimulated lung macrophages (MH-S). Anti-inflammatory parameters of HEBI were evaluated usingWestern blots, ELISA, RT-qPCR, and MTT assays. According to the results, HEBI at concentrations between 31.3 and 125 μg/mL reduced UPM-induced NO, PGE2, and pro-inflammatory cytokine production via blocking the downstream signal transduction of NF-κB and MAPKs. Specifically, HEBI down-regulated the mRNA expression levels of Toll-like receptors 2 and 4, which are well-known NF-κB and MAPKs stimulators. Taken together, HEBI is a potential candidate to develop functional foods and active ingredients in cosmeceuticals because of its profound effects against UPM-induced inflammation in MH-S macrophages.
목차
1. Introduction
2. Materials and Methods
2.1. Chemicals and Reagents
2.2. Purification and Isolation of HEBI from S. horneri
2.3. Estimation of UPM
2.4. Cell Culture and Sample Treatment
2.5. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium Bromide (MTT) Assay
2.6. Determination of NO Secretion Levels
2.7. Determination of PGE2 and Pro-Inflammatory Cytokine Secretion
2.8. Western Blot Analysis
2.9. Quantitative RT-PCR
2.10. Statistical Analysis
3. Results
3.1. Composition of UPM
3.2. Effect of UPM on Viability and NO Secretion of MH-S Macrophages
3.3. Effect of HEBI on the Viability of MH-S Macrophages
3.4. HEBI Down-Regulated UPM-Induced Cell Death, NO, and PGE2 Release in MH-S Cells
3.5. HEBI Down-Regulated UPM-Induced iNOS and COX2 Production
3.6. HEBI Down-Regulated UPM-Stimulated Pro-Inflammatory Cytokine Secretion
3.7. Inhibitory Effect of HEBI against UPM-Induced TLR Activations (RT-qPCR)
3.8. Suppressive Effect of HEBI in UPM-Induced NF-κB Activation
3.9. HEBI Inhibits MAPK Phosphorylation in UPM-Exposed MH-S Cells
4. Discussion
5. Conclusions
References
