• International Journal of Oral Biology
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• v.39 no.4
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• pp.221-228
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• 2014

Glucosamine is commonly taken by the elderly without prescription as a nutritional supplement to attenuate the progression or symptoms of osteoarthritis. Previous studies demonstrated that glucosamine shows anti-inflammatory effects in tissues such as blood vessels and the heart. However, there have been few reports about the effects of glucosamine on oral inflammatory diseases. Therefore, in this study, the effects of glucosamine on lipopolysaccharide (LPS)-induced inflammatory responses were investigated using human periodontal ligament fibroblasts (HPDLFs). HPDLFs were incubated in the presence and absence of glucosamine (10 mM) for 24 h, followed by treatment with E. coli LPS (100 ng/ml) or vehicle. Quantitative RT-PCR and ELISA results showed that LPS exposure significantly increased the levels of IL-6 and IL-8 mRNA and protein, while the effect was significantly suppressed by glucosamine treatment. Glucosamine did not attenuate, but slightly increased, the LPS-induced activation of mitogen activated kinases (ERK, p38, JNK). However, it suppressed the LPS-induced increase in the DNA binding affinity and transcriptional activity of NF-${\kappa}B$. These results suggest that glucosamine exerts anti-inflammatory effects on HPDLFs exposed to LPS via inhibition of NF-${\kappa}B$ activity, necessitating further studies using animal periodontitis models.

• Toxicological Research
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• v.27 no.2
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• pp.71-76
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• 2011

We demonstrate that baicalein, a bioactive flavonoid originally isolated from Scutellaria baicalensis, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Treatment of peritoneal macrophages and RAW 264.7 cells with baicalein inhibited LPS-stimulated nitric oxide production in a dose-related manner. Immunohistochemical staining of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunostaining of p65, EMSA, and reporter gene assay showed that baicalein inhibited NF-${\kappa}$B nuclear translocation, DNA binding, and transcriptional activation, respectively. Collectively, these series of experiments indicate that baicalein inhibits iNOS gene expression by blocking NF-${\kappa}$B nuclear translocation. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of baicalein on iNOS suggest that baicalein may represent a useful anti-inflammatory agent.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.84-95
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• 2003

Objective : This study was carried out to investigate the effects of Kamisopunghwalhyeol-tang (Jiaweishujenghuoxie-tang; Kami-SPHHT) on the immunity responses of the Synoviocytes isolated from the patients on rheumatoid arthritis. Methods : Cells were stimulated by $Interleukin-1{\beta}$ and Tumor Necrosis $Factor-{\alpha}$ in the presence or absence of Kami-SPHHT, and then induced cytokine mRNA levels were determined by RT-PCR and real-time quantitative RT-PCR. Results : Levels of $IL-1{\beta},{\;}IL-6,{\;}TNF-{\alpha}$, COX-2, and NOS II mRNA expressions significantly decreased in Kami-SPHHT treated cells compared to non-treated control cells. Also, DNA-binding activity of $NF-{\kappa}B$ and AP-l decreased in Kami- SPHHT treated hFLSs. Conclusion : These results suggest that Kami-SPHHT may be involved in anti-inflammatory reactions by inducing cytokine gene expression in synoviocytes, and further in vivo examination on its efficacy can provide potential application for the treatment of rheumatoid arthritis.

• Bulletin of the Korean Chemical Society
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• v.34 no.4
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• pp.1165-1169
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• 2013

To elucidate the role of PKG isoforms in transcriptional control of cyclin D1, we employed a series of expression vectors of PKG $1{\alpha}$ and PKG $1{\beta}$ which encode HA-tagged wild type and constitutively active (SD and ${\Delta}N$) mutants. Our present study demonstrates that both the constitutively active mutants of PKG $1{\beta}$ downregulate the transcription of cyclin D1 when transiently transfected in NIH3T3 cells, whereas PKG $1{\alpha}$ mutants show weak inhibition. We further studied the transcriptional regulators of cyclin D1, such as, c-fos, NF-${\kappa}B$, and CRE by using the luciferase reporter assay. Constitutively active mutants of PKG $1{\beta}$ showed marked transcriptional downregulation of c-fos in NIH3T3 cells, whereas PKG $1{\alpha}$ downregulated c-fos to a lesser extent. We also found that the constitutively active mutants of PKG negatively regulated the activation of NF-${\kappa}B$ and CRE, suggesting their involvement in the regulation of cyclin D1.

• BMB Reports
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• v.52 no.6
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• pp.409-414
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• 2019

Natural compounds isolated from medicinal herbs and plants have immense significance in maintaining bone health. Hydrolysable tannins have been shown to possess a variety of medicinal properties including antiviral, anticancer, and anti-osteoclastogenic activities. As a part of a study on the discovery of alternative agent against skeletal diseases, we isolated a hydrolysable tannin, 2-O-digalloyl-1,3,4,6-tetra-O-galloyl-${\beta}$-D-glucose (DTOGG), from Galla Rhois and examined the effect on osteoclast formation and function. We found that DTOGG significantly inhibited receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL)-induced osteoclast differentiation by downregulating the expression of the key regulator in osteoclastogenesis as well as osteoclast-related genes. Analysis of RANKL/RANK signaling revealed that DTOGG impaired activation of $I{\kappa}B{\alpha}$ and p65 in the nuclear factor kappa-lightchain-enhancer of activated B cells (NF-${\kappa}B$) signaling pathway. Furthermore, DTOGG reduced bone resorbing activity of osteoclasts, compared to the vehicle-treated control. These results suggest that DTOGG could be a useful natural compound to manage osteoclast-mediated skeletal diseases.

• 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.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.195.3-196
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• 2003

In this study, we investigated the molecular pathways targeted by platycodin D, which could involve apoptosis in immortalized human keratinocytes (HaCaT). We demonstrated that platycodin D-mediated apoptosis of HaCaT cells exhibited representative features, including DNA fragmentation, caspase-3, caspase-8 activation, and upregulation of Fas and FasL expression, but not p53 activation. To investigate the events involved in activation-induced FasL upregulation, we have examined mRNA accumulation, protein expression, and NF-$\kappa$B activity to elucidate transcription level in the HaCaT cell line treated with platycodin D. (omitted)

• Biomedical Science Letters
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• v.20 no.2
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• pp.96-102
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• 2014

Staphylococcal enterotoxin B (SEB) is bacterial toxin that induces the activation of immune cells. Because the inhibition of pro-inflammatory effect of SEB can resolve the inflammation, I determined the influence of functional or structural change of SEB on immune cells. The post translational modification of protein occurs through carbamylation. Carbamylation can change the structure of proteins and can modify the biological activity of protein. In the present study, I investigated the effect of carbamylated SEB (CSEB) on the inflammatory response mediated by LPS in HL-60 cells. To determine the anti-inflammatory effect of CSEB, I produced carbamylated SEB using potassium cyanate (KCN) and then examined whether CSEB involved in cytokine releases and apoptosis of LPS-stimulated HL-60 cells. Although CSEB had not any effect on the LPS-stimulated HL-60 cells, the protein levels of IL-8, TNF-${\alpha}$ and IL-$1{\beta}$ were significantly decreased by CSEB without cytotoxicity. CSEB also blocked Akt and NF-${\kappa}B$ activation. These results indicate that the suppressive effect of CSEB in LPS-stimulated cytokine releases is occurred by inhibition of Akt and NF-${\kappa}B$ activity. Through further studies, CSEB may be used as anti-inflammatory molecule that makes the immune system more efficient.

• BMB Reports
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• v.46 no.4
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• pp.201-206
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• 2013

Sulforaphane [1-isothiocyanato-4-(methylsulfinyl)-butane] is an isothiocyanate found in some cruciferous vegetables, especially broccoli. Sulforaphane has been shown to display anti-cancer properties against various cancer cell lines. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. In this study, we investigated the effect of sulforaphane on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced MMP-9 expression and cell invasion in MCF-7 cells. TPA-induced MMP-9 expression and cell invasion were decreased by sulforaphane treatment. TPA substantially increased NF-${\kappa}B$ and AP-1 DNA binding activity. Pre-treatment with sulforaphane inhibited TPA-stimulated NF-${\kappa}B$ binding activity, but not AP-1 binding activity. In addition, we found that sulforaphane suppressed NF-${\kappa}B$ activation, by inhibiting phosphorylation of $I{\kappa}B $ in TPA-treated MCF-7 cells. In this study, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by sulforaphane was mediated by the suppression of the NF-${\kappa}B$ pathway in MCF-7 cells.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2001.10b
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• pp.128-129
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• 2001