The present study evaluated the effects of (–)-loliolide isolated from Sargassum horneri (S. horneri) against oxidative stress and inflammation, and its biological mechanism in interferon (IFN)-γ/tumor necrosis factor (TNF)-α-stimulated HaCaT keratinocytes. The results showed that (–)-loliolide improved the cell viability by reducing the production of intracellular reactive oxygen species (ROS) in IFN-γ/TNF-α-stimulated HaCaT keratinocytes. In addition, (–)-loliolide effectively decreased the expression of inflammatory cytokines (interleukin (IL)-4 IL-6, IL-13, IFN-γ and TNF-α) and chemokines (CCL11 (Eotaxin), macrophage-derived chemokine (MDC), regulated on activation, normal T cell expressed and secreted (RANTES), and thymus and activation-regulated chemokine (TARC)), by downregulating the expression of epidermal-derived initial cytokines (IL-25, IL-33 and thymic stromal lymphopoietin (TSLP)). Furthermore, (–)-loliolide suppressed the activation of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling, whereas it activated nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Interestingly, the cytoprotective effects of (–)-loliolide against IFN-γ/TNF-α stimulation were significantly blocked upon inhibition of HO-1. Taken together, these results suggest that (–)-loliolide effectively suppressed the oxidative stress and inflammation by activating the Nrf2/HO-1 signaling in IFN-γ/TNF-α-stimulated HaCaT keratinocytes.

Sargassum horneri is a well-known edible brown alga that is widely abundant in the sea near China, Korea, and Japan and has a wide range of bioactive compounds. Fucosterol (FST), which is a renowned secondary metabolite in brown algae, was extracted from S. horneri to 70% ethanol, isolated via high-performance liquid chromatography (HPLC), followed by the immiscible liquid-liquid separation, and its structure was confirmed by NMR spectroscopy. The present study was undertaken to investigate the effects of FST against oxidative stress, inflammation, and its mechanism of action in tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated human dermal fibroblast (HDF). FST was biocompatible with HDF cells up to the 120 μM dosage. TNF-α/IFN-γ stimulation significantly decreased HDF viability by notably increasing reactive oxygen species (ROS) production. FST dose-dependently decreased the intracellular ROS production in HDFs. Western blot analysis confirmed a significant increment of nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) involvement in FST-treated HDF cells. In addition, the downregulation of inflammatory mediators, molecules related to connective tissue degradation, and tissue inhibitors of metalloproteinases were identified. TNF-α/IFN-γ stimulation in HDF cells increased the phosphorylation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) mediators, and its phosphorylation was reduced with the treatment of FST in a dose-dependent manner. Results obtained from western blot analysis of the NF-κB nuclear translocation were supported by immunocytochemistry results. Collectively, the outcomes suggested that FST significantly upregulates the Nrf2/HO-1 signaling and regulates NF-κB/MAPK signaling pathways to minimize the inflammatory responses in TNF-α/IFN-γ-stimulated HDF cells.

The health benefit of brown seaweeds has been proclaimed for centuries, particularly in Asian countries. A brown seaweed Sargassum horneri has been suggested to have immune-boosting and anti-inflammatory/immune-regulatory effects, but their mechanism is still elusive. This study researches the immunological effect of 70% ethanol extract of S. horneri (SHE) on unstimulated and Con A-stimulated murine splenocytes. When treated alone, SHE had an immune stimulatory effect on CD3e+ CD4+ T-helper cells, CD3e+ CD8+ cytotoxic T cells, CD45+ CD11b+ macrophages, Ly-6C+ Ly-6 G+ granulocytes, and Ly6 G- Ly6Clow eosinophils. Furthermore, SHE enhanced wide spectrum of Th cytokines such as TNF-α, IFN-γ (Th1), IL-4, IL-5, IL-13 (Th2), and IL-6 (Th17), which also stimulated the macrophage polarizing cytokines and enhanced macrophage derived cytokine secretion. SHE in Con A (5 μg/mL) stimulated cells decreased T-helper, cytotoxic T cells, granulocytes, eosinophils, and monocytes. These results signify the potential immuno-modulatory effect of SHE which can be developed as a therapeutic agent in immuno-compromised individuals.

Among the different kinds of pollution, air pollution continues to increase globally. East Asia is considered to be significantly affected. As a result, the populations in these regions face serious health issues including respiratory disorders. This study investigated the impact of fine dust (FD) particles (CRM No. 28) on macrophage cells as a model for alveolar lung cells. The research focused on inflammation and oxidative stress induced by FD and Sargassum horneri (Turner) C. Agardh ethanol extract (SHE) as a potential treatment. S. horneri is a type of brown algae that has demonstrated anti-inflammatory effects against RAW 264.7 macrophages in previous studies. MTT, Griess, ELISA, western blotting, and mRNA expression analyses using PCR techniques were used in this study. The optimum FD concentration was determined to be 125 μg mL− 1. FD particles stimulated inflammatory mediators production (iNOS, COX-2, and PGE2) and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), leading to NO production. These mediators were dose-dependently downregulated by treatment with SHE. IL-6 and TNF-α were identified as biomarkers for FD. SHE treatment induced HO-1 and Nrf2 activity in a dose-dependent manner under FD stimulation. This confirmed the cytoprotective effect against oxidative stress induced via FD. Furthermore, treatment of the cells with a p38 MAPK inhibitor (SB202190) induced FD-stimulated NO production. The results suggest that SHE increases macrophage cellular resistance to FD-induced inflammation and oxidative stress, probably via the p38 MAPK pathway and Nrf2/HO-1 expression.