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Background. Magnoliae flos is the dried flower bud of Magnolia biondii and related plants. It has been used as a medicinal herb for the treatment of rhinitis, sinusitis, and sinus headaches. Nevertheless, the effects of Magnoliae flos in microbial infection or sepsis remain unclear. In this study, we investigated the anti-inflammatory effects of Magnoliae flos water extract (MF) in lipopolysaccharide- (LPS-) induced septic mice and LPS-stimulated RAW264.7 macrophages. Results. We found that MF reduced the mortality of LPS-challenged mice. Enzyme immunoassays and reverse transcription polymerase chain reaction analysis revealed that MF administration attenuated mRNA expression and protein production of proinflammatory mediators, including cyclooxygenase 2, inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6. In parallel to these results in mice, pretreatment with MF suppressed the LPS-induced production of proinflammatory mediators in RAW264.7 macrophages. In addition, we found that MF exerted its suppressive effects by inhibiting the activation of the mitogen-activated protein kinase, nuclear factor-κB, and signal transducer and activator of transcription pathways at the protein level. Conclusion. MF could be a potential therapeutic agent for regulating excessive inflammatory responses in sepsis.

Seaweed fulvescens (SF) is a green alga rich in chlorophyll with unique flavor and taste. It is also called Maesaengi which has antioxidant and other physiological activities. In the present study, we evaluated the therapeutic effects of SF in a mouse model of Dermatophagoides farinae body-induced atopic dermatitis (AD) and in tumor necrosis factor-α and interferon-γ-stimulated HaCaT keratinocytes. SF treatment (200 mg/mouse) inhibited the development of AD symptoms, compared to that in the control group, as evidenced from the improved dorsal skin lesion, reduced thickness and infiltration of inflammatory cells and smaller lymph nodes, and reduced levels of proinflammatory cytokines. In HaCaT keratinocytes, SF (10, 25, and 50 μg/mL) suppressed the production of proinflammatory cytokines in a dose-dependent manner. In addition, SF reduced the phosphorylation of signal transducer and activator of transcription 1, which is one of the major signaling molecules involved in cellular inflammation. These results suggested that SF could be a potential therapeutic alternative for the treatment of AD.