• Toxicological Research
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• v.28 no.4
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• pp.255-262
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• 2012

Inflammation is the immune system's response to infection and injury-related disorders, and is related to pro-inflammatory factors (NO, $PGE_2$, cytokines, etc.) produced by inflammatory cells. Atopic dermatitis (AD) is a representative inflammatory skin disease that is characterized by increasing serum levels of inflammatory chemokines, including macrophage-derived chemokine (MDC). Carpinus tschonoskii is a member of the genus Carpinus. We investigated the anti-inflammatory activity of C. tschonoskii by studying the effects of various solvent fractions prepared from its leaves on inflammatory mediators in HaCaT and RAW264.7 cells. We found that the chloroform fraction of C. tschonoskii inhibited MDC at both the protein and mRNA levels in HaCaT cells, acting via the inhibition of STAT1 in the IFN-${\gamma}$ signaling pathway. In addition, the chloroform fraction significantly suppressed the expression of inflammatory factors induced by lipopolysaccharide stimulation, except COX-2 and TNF-${\alpha}$. These results suggest that the chloroform fraction of C. tschonoskii leaves may include a component with potential anti-inflammatory activity.

• Nutrition Research and Practice
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• v.8 no.3
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• pp.249-256
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• 2014

BACKGROUND/OBJECTIVES: The traditional Korean diet is plant-based and rich in antioxidants. Previous studies have investigated the potential health benefits of individual nutrients of Korean foods. However, the cumulative effects of a Korean diet on inflammation remain poorly understood. Therefore, the aim of this study was to investigate the anti-inflammatory effects of a plant-based Korean diet. MATERIALS/METHODS: Using data from the Fifth Korean National Health and Nutrition Examination Survey, 75 individual plant food items were selected which represent over 1% of the total diet intake of the Korean diet. These items were classified into ten different food groups, and the vegetable (Veg) and fruit (Fruit) groups were studied based on their high antioxidant capacity. For comparison, a mixture of all ten groups (Mix) was prepared. To produce a model of inflammation with which to test these Veg, Fruit, and Mix plant-based Korean food extracts (PKE), RAW264.7 macrophages were treated with lipopolysaccharide (LPS). RESULTS: Levels of nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$), as well as protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were found to be lower following PKE treatment. Furthermore, PKE treatment was found to suppress tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) via the nuclear transcription factor kappa-B ($NF-{\kappa}B$) signaling pathway. Overall, the Mix group exhibited the greatest anti-inflammatory effects compared with Veg and Fruit PKE group. CONCLUSIONS: Inhibition of LPS-induced pro-inflammatory mediators by the PKE tested was found to involve an inhibition of NF-kB activation. Moreover, PKE tested have the potential to ameliorate various inflammation-related diseases by limiting the excessive production of pro-inflammatory mediators.

• Preventive Nutrition and Food Science
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• v.16 no.4
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• pp.299-306
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• 2011

The present study was designed to evaluate the inhibitory effects of fermented Liriope platyphylla extract on the production of inflammation-related mediators (NO, ROS, NF-${\kappa}B$, iNOS and COX-2) and pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6) in lipopolysaccharide-stimulated RAW 264.7 macrophages. Freeze-dried Liriope platyphylla was fermented by Saccharomyces cerevisiae and extracted with 70% ethanol. In lipopolysaccharide-stimulated macrophage cells, the treatment with fermented Liriope platyphylla extract decreased the generation of intracellular reactive oxygen species dose-dependently and increased antioxidant enzyme activities, including superoxide dismutase, catalase and glutathione peroxidase. Fermented Liriope platyphylla extract also inhibited NO production in lipopolysaccharide-stimulated RAW 264.7 cell. The expressions of NF-${\kappa}B$, iNOS, COX-2 and pro-inflammatory cytokines were inhibited by the treatment with fermented Liriope platyphylla extract. Thus, this study shows the fermented Liriope platyphylla extract could be effective at inhibiting the inflammation process.

• Molecules and Cells
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• v.45 no.6
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• pp.353-361
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• 2022

Chronic rhinosinusitis (CRS) is a multifactorial, heterogeneous disease characterized by persistent inflammation of the sinonasal mucosa and tissue remodeling, which can include basal/progenitor cell hyperplasia, goblet cell hyperplasia, squamous cell metaplasia, loss or dysfunction of ciliated cells, and increased matrix deposition. Repeated injuries can stimulate airway epithelial cells to produce inflammatory mediators that activate epithelial cells, immune cells, or the epithelial-mesenchymal trophic unit. This persistent inflammation can consequently induce aberrant tissue remodeling. However, the molecular mechanisms driving disease within the different molecular CRS subtypes remain inadequately characterized. Numerous secreted and cell surface proteins relevant to airway inflammation and remodeling are initially synthesized as inactive precursor proteins, including growth/differentiation factors and their associated receptors, enzymes, adhesion molecules, neuropeptides, and peptide hormones. Therefore, these precursor proteins require post-translational cleavage by proprotein convertases (PCs) to become fully functional. In this review, we summarize the roles of PCs in CRS-associated tissue remodeling and discuss the therapeutic potential of targeting PCs for CRS treatment.

• Korean Journal of Oriental Medicine
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• v.8 no.1
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• pp.65-74
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• 2002

Inflammation is a disease that continues to afflict large numbers of people and may cause other diseases, for example, rheumatoid arthritis, colon cancer, etc. prostaglandins(PGs), one of arachidonic acid metabolites, are major chemical mediators in the process of inflammation. In traditional herbal medicine, many kinds of herbal drugs have been widely used for the treatment of inflammation. So, we analyzed many publications until 2001 which worked on inhibition of $PGE_2$ synthesis by cyclooxygenase-2 (COX-2) with herbs and herb oriented single compounds. And then we tried to make interpretations of herbal traditional prescriptions for inflammation. There are significant correlations between herbal medicine prescribed and inhibitions of COX-2 activity. From our efforts and further researches, we expect to develop new-inflammatory herbal drugs which have more efficacy and fewer side effects.

• Biomolecules & Therapeutics
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• v.31 no.5
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• pp.473-483
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• 2023

Many cancers arise from sites of chronic inflammation, which creates an inflammatory microenvironment surrounding the tumor. Inflammatory substances secreted by cells in the inflammatory environment can induce the proliferation and survival of cancer cells, thereby promoting cancer metastasis and angiogenesis. Therefore, it is important to identify the role of inflammatory factors in cancer progression. This review summarizes the signaling pathways and roles of C-reactive protein (CRP) in various cancer types, including breast, liver, renal, and pancreatic cancer, and the tumor microenvironment. Mounting evidence suggests the role of CRP in breast cancer, particularly in triple-negative breast cancer (TNBC), which is typically associated with a worse prognosis. Increased CRP in the inflammatory environment contributes to enhanced invasiveness and tumor formation in TNBC cells. CRP promotes endothelial cell formation and angiogenesis and contributes to the initiation and progression of atherosclerosis. In pancreatic and kidney cancers, CRP contributes to tumor progression. In liver cancer, CRP regulates inflammatory responses and lipid metabolism. CRP modulates the activity of various signaling molecules in macrophages and monocytes present in the tumor microenvironment, contributing to tumor development, the immune response, and inflammation. In the present review, we overviewed the role of CRP signaling pathways and the association between inflammation and cancer in various types of cancer. Identifying the interactions between CRP signaling pathways and other inflammatory mediators in cancer progression is crucial for understanding the complex relationship between inflammation and cancer.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.5
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• pp.486-493
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• 2014

Adipocytes are endocrine cells that release bioactive mediators called adipokines. In condition of obesity characterized by low-grade chronic inflammation, adipocytes release inflammatory adipokines, which is related to insulin resistance. Bojungchiseub-tang (BJCST) has been used in symptoms and signs of edema, dampness-phlegm, kidney failure, and so on in Korean medicine. BJCST is also expected to have anti-obesity activities. In the present study, we examined whether BJCST modulate the production of inflammatory adipokines and the activations of the mitogen-activated protein kinases (MAPK) signaling pathway related to induce adipocyte inflammation to elucidate the effects and its mechanism of BJCST on lowering the content of inflammatory adipokines in 3T3-L1 adipocytes. As a result, BJCST suppressed the production of proinflammatory cytokines, tumor necrosis factor (TNF) $-{\alpha}$, interleukin (IL) $-1{\beta}$, IL-6, interferon (IFN) -${\gamma}$, granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), and the production of other inflammatory mediators, prostaglandin $E_2(PGE_2)$ and nitric oxide(NO)viadownregulationofcyclooxygenase-2(COX-2)andinducible NO synthase (iNOS) gene expressions. In addition, BJCST decreased the phosphorylation of MAPK that promotes the production of inflammatory adipokines in 3T3-L1 mature adipocytes. In conclusion, BJCST could regulate the production of inflammatory adipokines and MAPK signaling pathway related to induction of adipose inflammation.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2010.10a
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• pp.13-13
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• 2010

In the present study, the chemical constituents of Artemisia fukudo essential oil (AFE) were investigated using GC-MS. The major constituents were ${\alpha}$-thujone (40.28%), ${\beta}$-thujone (12.69%), camphor (6.95%) and caryophyllene (6.01%). We also examined the effects of AFE on the production of nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-IL-$1{\beta}$ (IL-$1{\beta}$), and IL-6 in lipopolysaccharide (LPS)-activated RAW 264.7 cells. Western blotting and RT-PCR analyses indicated that AFE has potent dose-dependent inhibitory effects on pro-inflammatory cytokines and mediators. We investigated the mechanism by which AFE inhibits NO and $PGE_2$ by examining the level of nuclear factor-${\kappa}B$ (NF-${\kappa}B$: p50 and p65) activation within the mitogen-activated protein kinase (MAPK: ERK, JNK and p38) pathway, which is an inflammation induced signal pathway in RAW 264.7 cells. AFE inhibited LPS-induced ERK, JNK and p38 phosphorylation. Furthermore, AFE inhibited the LPS-induced phosphorylation and degradation of $I{\kappa}B-{\alpha}$, which is required for the nuclear translocations of the p50 and p65 NF-${\kappa}B$ subunits in RAW 264.7 cells. Our results suggest that AFE might exert an anti-inflammatory effect by inhibiting the expression of pro-inflammatory cytokines. Such an effect is mediated by a blocking of NF-${\kappa}B$ activation which consequently inhibits the generation of inflammatory mediators in RAW 264.7 cells. AFE may be useful for treating inflammatory diseases.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.291-297
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• 2015

An oral environment is constantly exposed to environmental factors and microorganisms. The periodontal ligament (PDL) fibroblasts within this environment are subject to bacterial infection and allergic reaction. However, how these condition affect PDL fibroblasts has yet to be elucidated. PDL fibroblasts were isolated from healthy donors. We examined using reverse transcription-polymerase chain reaction and measuring the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$). This study investigated the receptors activated by exogenous bacterial pathogens (Lipopolysaccharide and peptidoglycan) and allergens (German cockroach extract and house dust mite) as well as these pathogenic mediators-induced effects on the intracellular $Ca^{2+}$ signaling in human PDL fibroblasts. Moreover, we evaluated the expression of pro-inflammatory cytokines (interleukin (IL)-$1{\beta}$, IL-6, and IL-8) and bone remodeling mediators (receptor activator of NF-${\kappa}B$ ligand and osteoprotegerin) and intracellular $Ca^{2+}$-involved effect. Bacterial pathogens and allergic mediators induced increased expression of pro-inflammatory cytokines, and these results are dependent on intracellular $Ca^{2+}$. However, bacterial pathogens and allergic mediators did not lead to increased expression of bone remodeling mediators, except lipopolysaccharide-induced effect on receptor activator of NF-${\kappa}B$ ligand expression. These experiments provide evidence that a pathogens and allergens-induced increase in $[Ca^{2+}]_i$ affects the inflammatory response in human PDL fibroblasts.

• Natural Product Sciences
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• v.15 no.4
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• pp.185-191
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• 2009

Intestinal epithelial cells (IEC) play an important role in the mucosal immune system. IEC-derived mediators of inflammatory cascades play a principal role in the development of colon inflammation. The aim of this study was to investigate the inhibitory effect of aqueous extracts of Schizandra chinensis fruits (SC-Ex) on the production of inflammatory mediators by the human colonic epithelial cells. HT-29 cells were stimulated with dextran sulfate sodium in the presence or absence of SC-Ex to examine the cytoprotection and production of IL-8 and reactive oxygen species (ROS). It was shown that dextran sulfate sodium (DSS) caused the reduction of cell viability and production of IL-8 and ROS in DSS-treated HT-29 cells. We observed that the treatment of SC-Ex protected significantly cell proliferation from DSS-induced damage in dose-dependent manner. SC-Ex (10 and 100 ${\mu}g$/ml) also suppressed DSS-induced production of IL-8 mRNA and protein. Moreover, DSS-induced ROS production was inhibited markedly by the treatment of 100 ${\mu}g$/ml SC-Ex. These results suggest that SC-Ex has the protective effects on DSS-induced cell damage and the release of inflammatory mediators in the intestinal epithelial cells.