• Journal of Microbiology and Biotechnology
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• v.33 no.8
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• pp.1057-1065
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• 2023

Inflammatory bowel disease (IBD), a chronic inflammatory disease, results from dysregulation of the immune responses. Some lactic acid bacteria (LAB), including Lactobacillus, alleviate IBD through immunomodulation. In this study, the anti-colitis effect of LAB isolated from human breast milk was investigated in a mouse model induced acute colitis with 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS remarkably increased weight loss, colon shortening, and colonic mucosal proliferation, as well as the expression levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β. Oral administration of LAB isolated from human breast milk resulted in a reduction in TNBS-induced colon shortening, as well as induced cyclooxygenase (COX)-2, nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB). In addition, LAB suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and thus showed an effect of suppressing the level of inflammation induced by TNBS. Furthermore, LAB alleviated gut microbiota dysbiosis, and inhibited intestinal permeability by increasing the expression of intestinal tight junction protein including ZO-1. Collectively, these results suggest that LAB isolated from human breast milk can be used as a functional food for colitis treatment by regulating NF-κB signaling, gut microbiota and increasing expression of intestinal tight junction protein.

• The Korea Journal of Herbology
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• v.27 no.1
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• pp.65-71
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• 2012

Objective : Nelumbinis Folium (NF) is used for diarrhea, headache and dizziness in traditional medicine. In this paper, we examined the anti-inflammatory effects of the methanol extract of NF in mouse macrophages. Methods : Peritoneal macrophages from thioglycollate medium-injected mice were cultured and stimulated with lipopolysaccharide(LPS) or LPS/interferon(IFN)-${\gamma}$ for viability assay, cytokine measurement and Western blotting. Results : NF methanol extract suppressed the levels of nitric oxide (NO) through reduction of inducible NO synthase in a concentration-dependent manner. The extract reduced LPS/IFN-${\gamma}$-stimulated STAT1 phosphorylation and LPS-induced $I{\kappa}B{\alpha}$ degradation through inhibition of $I{\kappa}B{\alpha}$ kinase activation. The extract also inhibited p38, JNK/SAPK and ERK1/2 activation. Conclusions : Our findings suggested that NF has anti-inflammatory activity, and have a potential for therapeutic application. Further research is required to investigate its anti-inflammatory active compounds.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.26 no.1
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• pp.50-62
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• 2013

Objective : Propionibacterium acnes (P. acnes) is a major pathogenic bacteria for acne vulgaris. This study was performed to evaluate the effects of Lithospermum erythrorhizon extracts on the inflammatory cytokines gene expression by P. acnes in human keratinocytes, HaCaT cell line. Methods : Anti-bacterial activity and cytotoxicity of LE extracts was analyzed by agar plate culture and XTT assay. The cytokines gene expressions were assessed by real time RT-PCR for IL-8, MCP-1 and TNF-${\alpha}$. During the cell culture and treatments, amounts of secreted TNF-${\alpha}$ were measured by ELISA. Translocation of transcription factor NF-${\kappa}B$ from cytoplasm into nucleus was observed by immunocytochemistry and confocal microscopy. Results : There were no anti-bacterial effects and cytotoxicity as high as $1,000{\mu}g/ml$ of LE extracts in XTT assay. Transcription levels of inflammatory cytokines, IL-8, MCP-1 and TNF-${\alpha}$ were increased by P. acnes in HaCaT. LE extracts decreased the upregulated gene transcription levels. However, amounts of secreted TNF-${\alpha}$ were similar in HaCaT cells with P. acnes and LE extracts. Translocation of NF-${\kappa}B$ into nucleus by P. acnes was significantly inhibited by LE extracts. Conclusions : From the results of this study, LE extracts have anti-inflammatory effects on HaCaT cells by P. acnes that decreased the mRNA expressions of IL-8, MCP-1 and TNF-${\alpha}$. This anti-inflammatory effects of LE extracts could provide the potential of therapeutic substance for acne vulgaris.

• Nutrition Research and Practice
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• v.9 no.1
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• pp.3-10
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• 2015

BACKGROUND/OBJECTIVES: Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. Previously, Sasa quelpaertensis leaves have been shown to mediate anti-inflammation and anti-cancer effects, although it remains unclear whether Sasa leaves are able to attenuate inflammation-related intestinal diseases. Therefore, the aim of this study was to investigate the anti-inflammatory effects of Sasa quelpaertensis leaf extract (SQE) using an in vitro co-culture model of the intestinal epithelial environment. MATERIALS/METHODS: An in vitro co-culture system was established that consisted of intestinal epithelial Caco-2 cells and RAW 264.7 macrophages. Treatment with lipopolysaccharide (LPS) was used to induce inflammation. RESULTS: Treatment with SQE significantly suppressed the secretion of LPS-induced nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), IL-6, and IL-$1{\beta}$ in co-cultured RAW 264.7 macrophages. In addition, expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and tumor necrosis factor (TNF)-${\alpha}$ were down-regulated in response to inhibition of $I{\kappa}B{\alpha}$ phosphorylation by SQE. Compared with two bioactive compounds that have previously been identified in SQE, tricin and P-coumaric acid, SQE exhibited the most effective anti-inflammatory properties. CONCLUSIONS: SQE exhibited intestinal anti-inflammatory activity by inhibiting various inflammatory mediators mediated through nuclear transcription factor kappa-B (NF-kB) activation. Thus, SQE has the potential to ameliorate inflammation-related diseases, including IBD, by limiting excessive production of pro-inflammatory mediators.

• BMB Reports
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• v.50 no.1
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• pp.25-30
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• 2017

In the central nervous system, viral infection can induce inflammation by up-regulating pro-inflammatory mediators that contribute to enhanced infiltration of immune cells into the central nervous areas. Celastrol is known to exert various regulatory functions, including anti-microbial activities. In this study, we investigated the regulatory effects and the mechanisms of action of celastrol against astrocytes activated with polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, as a model of pro-inflammatory mediated responses. Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. Furthermore, celastrol significantly suppressed poly(I:C)-induced activation of the $NF-{\kappa}B$ signaling pathway. These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/$NF-{\kappa}B$ in astrocytes.

• Fisheries and Aquatic Sciences
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• v.22 no.3
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• pp.7.1-7.10
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• 2019

Sargassum serratifolium ethanolic extract has been known for strong antioxidant and anti-inflammatory properties. We prepared hexane fraction from the ethanolic extract of S. serratifolium (HSS) to improve biological activities. In this study, we investigated the effects of HSS on the inhibition of tumor necrosis factor (TNF)-${\alpha}$-induced monocyte adhesion to human umbilical vein endothelial cells (HUVECs). We found that HSS suppressed the production of cell adhesion molecules such as intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 in TNF-${\alpha}$-induced HUVECs. Moreover, TNF-${\alpha}$-induced production of monocyte chemoattractant protein 1 and keratinocyte chemoattractant was inhibited by HSS treatment. HSS suppressed TNF-${\alpha}$-induced nuclear factor kappa B ($NF-{\kappa}B$) activation via preventing proteolytic degradation of inhibitor ${\kappa}B-{\alpha}$. HSS induced the production of heme oxygenase 1 via translocation of Nrf2 into the nucleus in TNF-${\alpha}$-treated HUVECs. Overall, HSS alleviated vascular inflammation through the downregulation of $NF-{\kappa}B$ activation and the upregulation of Nrf2 activation in TNF-${\alpha}$-induced HUVECs. These results indicate that HSS may be used as therapeutic agents for vascular inflammatory disorders.

• Molecules and Cells
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• v.38 no.11
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• pp.982-990
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• 2015

Exposure of the skin to ultraviolet radiation can cause skin damage with various pathological changes including inflammation. In the present study, we identified the skin-protective activity of 1,2,3,4,6-penta-O-galloyl-${\beta}$-D-glucose (pentagalloyl glucose, PGG) in ultraviolet B (UVB) radiation-induced human dermal fibroblasts and mouse skin. PGG exhibited antioxidant activity with regard to intracellular reactive oxygen species (ROS) generation as well as ROS and reactive nitrogen species (RNS) scavenging. Furthermore, PGG exhibited anti-inflammatory activity, inhibiting the activation of nuclear factor-kappaB (NF-${\kappa}B$) and mitogen-activated protein kinase (MAPK) signaling, resulting in inhibition of the expression of pro-inflammatory mediators. Topical application of PGG followed by chronic exposure to UVB radiation in the dorsal skin of hairless mice resulted in a significant decrease in the progression of inflammatory skin damages, leading to inhibited activation of NF-${\kappa}B$ signaling and expression of pro-inflammatory mediators. The present study demonstrated that PGG protected from skin damage induced by UVB radiation, and thus, may be a potential candidate for the prevention of environmental stimuli-induced inflammatory skin damage.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.55-61
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• 2014

Panax ginseng is a medicinal herb that is used worldwide. Its medicinal effects are primarily attributable to ginsenosides located in the root, leaf, seed, and flower. The flower buds of Panax ginseng (FBPG) are rich in various bioactive ginsenosides, which exert immunomodulatory and anti-inflammatory activities. The aim of the present study was to assess the effect of 18 ginsenosides isolated from steamed FBPG on the transcriptional activity of NF-${\kappa}B$ and the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated target genes in liver-derived cell lines. Noticeably, the ginsenosides $Rk_3$ and $Rs_4$ exerted the strongest activity, inhibiting NF-${\kappa}B$ in a dose-dependent manner. SF and $Rg_6$ also showed moderately inhibitory effects. Furthermore, these four compounds inhibited the TNF-${\alpha}$-induced expression of IL8, CXCL1, iNOS, and ICAM1 genes. Consequently, ginsenosides purified from steamed FBPG have therapeutic potential in TNF-${\alpha}$-mediated diseases such as chronic hepatic inflammation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.3
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• pp.410-415
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• 2010

The purpose of this study was to investigate the anti-inflammatory effects of aqueous extract from Belamcanda chinensis (BC) on the RAW 264.7 cells. To evaluate the anti-inflammatory effects of BC, we examined the cytokine productions including nitric oxide (NO), interleukin (IL)-1b, IL-6 and tumor necrosis factor-a (TNF-a) in lipopolysaccharide (LPS)-induced RAW 264.7 cells and also inhibitory mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-kB) using Western blot. BC inhibited LPS-induced production of NO, IL-6 and TNF-a but not of IL-1b in RAW 264.7 cells. BC respectively inhibited the activation of MAPKs such as c-Jun NH2-terminal kinase (JNK) and p38 but not of extracelluar signal-regulated kinase (ERK 1/2) and NF-kB in the LPS-stimulated RAW 264.7 cells. Taken together, Our results showed that BC down-regulated LPS-induced NO, IL-6 and TNF-a productions mainly through JNK and p38 MAPK pathway.

• Parasites, Hosts and Diseases
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• v.54 no.2
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• pp.123-132
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• 2016

Trichomonas vaginalis causes the most prevalent sexually transmitted infection worldwide. Trichomonads have been detected in prostatic tissues from prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer. Chronic prostatic inflammation is known as a risk factor for prostate enlargement, benign prostatic hyperplasia symptoms, and acute urinary retention. Our aim was to investigate whether T. vaginalis could induce inflammatory responses in cells of a benign prostatic hyperplasia epithelial cell line (BPH-1). When BPH-1 cells were infected with T. vaginalis, the protein and mRNA of inflammatory cytokines, such as CXCL8, CCL2, IL-$1{\beta}$, and IL-6, were increased. The activities of TLR4, ROS, MAPK, JAK2/STAT3, and NF-${\kappa}B$ were also increased, whereas inhibitors of ROS, MAPK, PI3K, NF-${\kappa}B$, and anti-TLR4 antibody decreased the production of the 4 cytokines although the extent of inhibition differed. However, a JAK2 inhibitor inhibited only IL-6 production. Culture supernatants of the BPH-1 cells that had been incubated with live T. vaginalis (trichomonad-conditioned medium, TCM) contained the 4 cytokines and induced the migration of human monocytes (THP-1 cells) and mast cells (HMC-1 cells). TCM conditioned by BPH-1 cells pretreated with NF-${\kappa}B$ inhibitor showed decreased levels of cytokines and induced less migration. Therefore, it is suggested that these cytokines are involved in migration of inflammatory cells. These results suggest that T. vaginalis infection of BPH patients may cause inflammation, which may induce lower urinary tract symptoms (LUTS).