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Duchesnea indica is known as false strawberry, is found in East Asia, and has numerous biological properties. The aim of this study was to investigate the anti-inflammatory effect of Duchesnea indica extract (DIE) on coal fly ash- (CFA-) induced inflammation in murine alveolar macrophages (MH-S). Following the induction of inflammation in MH-S cells by CFA, nitric oxide (NO) was measured to evaluate the anti-inflammatory property of DIE. Cell viability and inflammatory gene expression were analyzed using polymerase chain reaction (PCR). The inflammatory pathway in MH-S cells was determined via western blotting and immunofluorescence (IF) analysis. Finally, the major components of the DIE were identified and separated through ultra-performance liquid chromatography (UPLC) and gas chromatography-mass spectrometry (GC-MS) analysis. Our results showed that the DIE dose-dependently inhibited the CFA-induced NO production in MH-S cells. Moreover, the DIE could suppress the CFA-induced proinflammatory mediators, such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). In addition, the inhibitory effect of the DIE on proinflammatory cytokines, including interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α), was detected with PCR. Moreover, the effect of the DIE on the nuclear factor-κB (NF-κB) pathway in CFA-activated MH-S cells was measured via western blotting. Furthermore, the inhibition of the phosphorylated NF-κB (p-NF-κB) translocation was analyzed using IF assay. The findings of this study indicated that the DIE potentially inhibited the CFA-induced inflammation by blocking the NF-κB inflammatory signaling pathway in MH-S cells and that the DIE might contain favorable anti-inflammatory compounds which may be effective in attenuating lung inflammation.

BackgroundGinseng (Panax ginseng) is a widely used traditional herbal supplement that possesses various health-enhancing efficacies. Various ginseng products are available in market, especially in the Korean peninsula, in the form of drinks, tablets, and capsules. The different ginseng types include the traditional red ginseng extract (RGE), white ginseng, and black red ginseng extract (BRGE). Their fermented and enzyme-treated products are also available. Different treatment regimens alter the bioavailability of certain compounds present in the respective ginseng extracts. Therefore, in this study, we aimed to compare the antioxidant and immune-stimulating activities of RGE, BRGE, and fermented red ginseng extract (FRGE).MethodsWe used an acetaminophen-induced oxidative stress model for investigating the reduction of oxidative stress by RGE, BRGE, and FRGE in Sprague Dawley rats. A cyclophosphamide-induced immunosuppression model was used to evaluate the immune-stimulating activities of these ginseng extracts in BALB/c mice.ResultsOur results showed that most prominently, RGE (in almost all experiments) exhibited excellent antioxidant effects via increasing superoxide dismutase, catalase, and glutathione peroxidase activities in the liver and decreasing serum 8-hydroxy-2′-deoxyguanosine, aspartate aminotransferase, and lactate dehydrogenase levels compared with the groups treated with FRGE and BRGE. Moreover, RGE significantly increased the number of white blood cells, especially T and B lymphocytes, and antibody-forming cells in the spleen and thymus, and it also activated a number of immune cell subtypes.ConclusionTaken together, these results indicate that RGE is the best supplement for consumption in everyday life for overall health-enhancing properties.

Coal fly dust (CFD)-induced asthma model is used as an ambient particulate matter model of serious pulmonary damage. We aimed to evaluate the effects of a combination of ginseng and Salvia plebeia R. Br extract (KGC-03-PS; KG3P) and its individual components (hispidulin, nepetin and rosmarinic acid) in a CFD-induced mouse model of airway inflammation (asthma). We also evaluated signal transduction by KG3P and its individual components in the alveolar macrophage cell line, MH-S cells. In vitro, KG3P and its individual components inhibited nitric oxide production and expression of pro-inflammatory mediators and cytokines (iNOS, COX-2, IL-1β, IL-6 and TNF-α) through the NF-κB and MAPK pathways in coal fly ash (CFA)-induced inflammation in MH-S cells. Moreover, in the CFD-induced asthma model in mice, KG3P and its predominant individual component, nepetin, inhibited Asymmetric Dimethyl arginine (ADMA) and Symmetric Dimethyl arginine (SDMA) in serum, and decreased the histopathologic score in the lungs. A significant reduction in the neutrophils and immune cells in BALF and lung tissue was demonstrated, with significant reduction in the expression of the pro-inflammatory cytokines. Finally, IRAK-1 localization was also potently inhibited by KG3P and nepetin. Thus, KG3P extract can be considered as a potent candidate for amelioration of airway inflammation.

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