Abstract
Acute lung injury (ALI) is a critical clinical condition with a high mortality rate. It is believed that the inflammatory storm is a critical contributor to the occurrence of ALI. Fucoxanthin is a natural extract from marine seaweed with remarkable biological properties, including antioxidant, anti-tumor, and anti-obesity. However, the anti-inflammatory activity of Fucoxanthin has not been extensively studied. The current study aimed to elucidate the effects and the molecular mechanism of Fucoxanthin on lipopolysaccharide-induced acute lung injury. In this study, Fucoxanthin efficiently reduced the mRNA expression of pro-inflammatory factors, including IL-10, IL-6, iNOS, and Cox-2, and down-regulated the NF-κB signaling pathway in Raw264.7 macrophages. Furthermore, based on the network pharmacological analysis, our results showed that anti-inflammation signaling pathways were screened as fundamental action mechanisms of Fucoxanthin on ALI. Fucoxanthin also significantly ameliorated the inflammatory responses in LPS-induced ALI mice. Interestingly, our results revealed that Fucoxanthin prevented the expression of TLR4/MyD88 in Raw264.7 macrophages. We further validated Fucoxanthin binds to the TLR4 pocket using molecular docking simulations. Altogether, these results suggest that Fucoxanthin suppresses the TLR4/MyD88 signaling axis by targeting TLR4, which inhibits LPS-induced ALI, and fucoxanthin inhibition may provide a novel strategy for controlling the initiation and progression of ALI.
Highlights
Acute lung injury (ALI) is a disease of pulmonary edema and respiratory failure caused by the injury of capillary endothelial cells and alveolar epithelial cells.It is a critical clinical disease with high mortality [1]
Western blot analysis showed that Fucoxanthin could dramatically reduce the protein expression of COX-2 and iNOS induced by LPS (Figure 2B), indicating that Fucoxanthin is a potential drug against inflammation in vitro
In order to further evaluate the anti-inflammatory activity of Fucoxanthin on LPS-stimulated macrophages, we examined its effect on the expression of pro-inflammatory cytokines stimulated by LPS, such as COX-2, iNOS, IL10, IL-6, tumor necrosis factor-α (TNF-α), and IL-1β
Summary
Acute lung injury (ALI) is a disease of pulmonary edema and respiratory failure caused by the injury of capillary endothelial cells and alveolar epithelial cells.It is a critical clinical disease with high mortality [1]. Acute lung injury (ALI) is a disease of pulmonary edema and respiratory failure caused by the injury of capillary endothelial cells and alveolar epithelial cells. As such, removing the excessive production of those cytokines by anti-inflammatory agents, including corticosteroids, such as methylprednisolone [4], dexamethasone [5], prednisolone [6], represented a promising strategy to prevent and treat ALI [7]. Most of these drugs have no beneficial effect on ALI patients because of their low efficacy and severe side effects. The treatment of ALI urgently needs new anti-inflammatory drugs with better efficacy and safety
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