###### Abstract  
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-\(\beta\)-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 using Western blots, ELISA, RT-qPCR, and MTT assays. According to the results, HEBI at concentrations between 31.3 and 125 ug/mL reduced UPM-induced NO, PGE2, and pro-inflammatory cytokine production via blocking the downstream signal transduction of NF-kB and MAPKs. Specifically, HEBI down-regulated the mRNA expression levels of Toll-like receptors 2 and 4, which are well-known NF-kB 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. lung macrophages; inflammation; oxidative stress; _Sargassum horneri_; particulate matter +
Footnote †: journal: Medical  
functions of the respiratory system, skin, and digestive tract. The sand storms originated in Mongolia and China's extensive arid and semiarid highlands carry a large amount of particulate matter to East-Asian countries such as South Korea and Japan [3]. In addition, coal-burning power plants, petroleum vehicles, and other industrial operations such as construction work also increase UPM concentration in the East-Asia region [4]. Studies have demonstrated that UPM can increase cancer cell development in the lungs [5]. Alveolar macrophages, such as MH-S, stay in the lower respiratory tract while phagocyte UPM particles reach the lower respiratory tract. Based on the particle size and heavy metal composition, UPM-exposed macrophages initiate inflammatory responses [6]. According to the previous studies, UPM act as inflammatory stimuli on macrophages. Recently, several studies reported that UPM could act as inflammatory stimuli in macrophages via stimulating inflammation-related signal cascades. The endotoxins presented in UPM particles were found to up-regulate the toll-like receptor (TLR)-4 dependent inflammatory responses via up-regulating pro-inflammatory cytokine secretion from MH-S murine lung macrophages. Moreover, PMs moved to the lower respiratory tract phagocytes via macrophages and then were removed by lysosome activation. As a result, the macrophage population in the lungs decreased, which further reduced the immunity in UPM-exposed lungs [7]. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-\(\kappa\)B) has been a key mediator in inflammatory diseases. The activation of NF-\(\kappa\)B is stimulated by factors such as LPS, viral infection, inflammatory cytokines (tumor necrosis factor-alpha and r interleukins), and UV irradiation [8]. The activation and translocation of NF-\(\kappa\)B proteins (p50 and p65) are strictly controlled by the inhibitor protein called IxB. Phosphorylation and subsequent degradation of IxB allow the activation and mobilization of NF-\(\kappa\)B to the nucleus [9]. In the cytoplasm, three forms of IxB identified and known as IxB-\(\alpha\), IxB-\(\beta\), and IxB-\(\epsilon\). Among those, only IxB-\(\alpha\) binds to p50 heterodimer and p50-p65 homodimer.