• International Journal of Industrial Entomology and Biomaterials
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• v.48 no.1
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• pp.13-18
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• 2024

The rice field grasshopper, Oxya chinensis sinuosa (OC), has traditionally been utilized in Korea for various purposes; however, its potential benefits in the context of osteoporosis remain unclear. The results revealed that OC ethanol extract (OCE) significantly inhibited the formation and activity of tartrate-resistant acid phosphatase (TRAP)-positive cells in receptor activator of nuclear factor-κB ligand (RANKL)-stimulated RAW264.7 cells. Furthermore, OCE, at concentrations ranging from 100 to 400 ㎍/mL, demonstrated a dose-dependent reduction in the protein expression of osteoclast-specific markers, including nuclear factor of activated T cell cytoplasmic 1, c-Src, and TRAP, when compared to RANKL stimulation alone. Additionally, OCE significantly inhibited RANKL-induced activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) but not the activation of extracellular signal-regulated kinase. Collectively, these results indicate that OCE suppresses osteoclastogenesis by attenuating the phosphorylation of p38 MAPK and JNK. Consequently, these findings suggest that OCE holds promise for the prevention of osteoporosis.

• Molecules and Cells
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• v.27 no.1
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• pp.113-118
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• 2009

In this study, we have shown the transcriptional regulation of the human GD3 synthase (hST8Sia I) induced by valproic acid (VPA) in human neuroblastoma SK-N-BE(2)-C cells. To elucidate the mechanism underlying the regulation of hST8Sia I gene expression in VPA-stimulated SK-N-BE(2)-C cells, we characterized the promoter region of the hST8Sia I gene. Functional analysis of the 5'-flanking region of the hST8Sia I gene by the transient expression method showed that the -1146 to -646 region, which contains putative binding sites for transcription factors c-Ets-1, CREB, AP-1 and NF-${\kappa}B$, functions as the VPA-inducible promoter of hST8Sia I in SK-N-BE(2)-C cells. Site-directed mutagenesis and electrophoretic mobility shift assay indicated that the NF-${\kappa}B$ binding site at -731 to -722 was crucial for the VPA-induced expression of hST8Sia I in SK-N-BE(2)-C cells. In addition, the transcriptional activity of hST8Sia I induced by VPA in SK-N-BE(2)-C cells was strongly inhibited by SP600125, which is a c-Jun N-terminal kinase (JNK) inhibitor, and $G{\ddot{O}}6976$, which is a protein kinase C (PKC) inhibitor, as determined by RT-PCR (reverse transcription-polymerase chain reaction) and luciferase assays. These results suggest that VPA markedly modulated transcriptional regulation of hST8Sia I gene expression through PKC/JNK signal pathways in SK-N-BE(2)-C cells.

• The Journal of Internal Korean Medicine
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• v.34 no.2
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• pp.204-214
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• 2013

Objectives : This study was designed to investigate the cellular and molecular mechanisms of anti-inflammatory activity of the water extract of Polygala tenuifolia Willd. (Pt-WE). Methods : Using lipopolysaccharide (LPS)-stimulated murine RAW264.7 cells, we examined inflammatory mediators such as nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase (COX)-2 and prostaglandin $E_2$ ($PGE_2$). Also, the inhibitory effect of Pt-WE on the activity of activator protein 1 (AP-1) and upstream signaling molecules was evaluated. To assess the protective effect of Pt-WE on hydrochloride/ethanol (HCl/EtOH)-induced gastric ulcer in mice, we compared Pt-WE (200 mg/kg) with ranitidine (50 mg/kg) treated mice's gastric mucosa, based on gross observations. Results : Pt-WE inhibited LPS-induced production of NO, $PGE_2$ in a dose-dependent manner, without causing cytotoxicity. Pt-WE suppressed AP-1 activation by reducing generations of both c-Jun and c-Fos. In addition, Pt-WE inhibited the p-MKK 4/7 (mitogen-activated protein kinase kinase 4/7) and p-JNK (c-Jun N-terminal kinase) 1 in LPS-stimulated RAW264.7 cells. HCl/EtOH-induced gastric ulcer lesions were inhibited by pre-treatment of Pt-WE based on gross observations. In addition, Pt-WE decreased the phosphorylation level of JNK. Conclusions : These results demonstrate that Pt-WE has anti-inflammatory and gastroprotective effects. Thus, Pt-WE may be used widely in treatment of not only neurodegenerative diseases but also inflammatory diseases.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.147-147
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• 2001

A previous study showed that sulfur amino acid deprivation (SAAD) potentiated cytotoxicity induced by arsenic (As) and that activation of ERKl/2, p38 kinase and JNK1 was responsible for the potentiation of As toxicity. In the present study, we found for the first time that deprenyl a selective monoamine oxidase B inhibitor prevented potentiation of As toxicity by SAAD in a dose-dependent manner.(omitted)

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.78-78
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• 2002

• Journal of Periodontal and Implant Science
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• v.47 no.2
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• pp.116-131
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• 2017

Purpose: The entry of bacteria or harmful substances through the epithelial seal of human gingival keratinocytes (HGKs) in the junctional epithelium (JE) is blocked by specialized intercellular junctions such as E-cadherin junctions (ECJs). However, the influence of roughened substrates, which may occur due to apical migration of the JE, root planing, or peri-implantitis, on the development of the ECJs of HGKs remains largely unknown. Methods: HGKs were cultured on substrates with varying levels of roughness, which were prepared by rubbing hydrophobic polystyrene dishes with silicon carbide papers. The activity of c-Jun N-terminal kinase (JNK) was inhibited with SP600125 or by transfection with JNK short hairpin RNA. The development of intercellular junctions was analyzed using scanning electron microscopy or confocal laser scanning microscopy after immunohistochemical staining of the cells for E-cadherin. The expression level of phospho-JNK was assessed by immunoblotting. Results: HGKs developed tight intercellular junctions devoid of wide intercellular gaps on smooth substrates and on rough substrates with low-nanometer dimensions (average roughness $[Ra]=121.3{\pm}13.4nm$), although the ECJs of HGKs on rough substrates with low-nanometer dimensions developed later than those of HGKs on smooth substrates. In contrast, HGKs developed short intercellular junctions with wide intercellular gaps on rough substrates with mid- or high-nanometer dimensions ($Ra=505.3{\pm}115.3nm$, $867.0{\pm}168.6nm$). Notably, the stability of the ECJs was low on the rough substrates, as demonstrated by the rapid destruction of the cell junction following calcium depletion. Inhibition of JNK activity promoted ECJ development in HGKs. JNK was closely associated with cortical actin in the regulation of ECJs in HGKs. Conclusions: These results indicate that on rough substrates with nanometer dimensions, the ECJs of HGKs develop slowly or defectively, and that this effect can be reversed by inhibiting JNK.

• Journal of Veterinary Clinics
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• v.28 no.6
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• pp.549-554
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• 2011

FK506 is a widespread immunosuppressive drug after liver transplantion in patients with advanced-stage hepatocellular carcinoma. Dexamethasone is frequently used as co-treatment in cytotoxic cancer therapy, e.g. to prevent nausea, to protect normal tissue or for other reasons. Our aim was to investigate antitumor effects of FK506 in Hep3B cells, one of differentiated human hepatocellular carcinoma cell lines and inhibitory effects of dexamethsone on FK506- induced antitumor effects. Cell injury was evaluated by biochemical assays as cell viability, lactate dehydrogenase (LDH) and reactive oxygen species (ROS) in Hep3B cells. Intracellular calcium concentration ([$Ca^{2+}$]i) and the level of activation of the c-Jun-N-terminal kinase (JNK) and the Bax protein in cultured Hep3B cells was measured. Exposure of 0.1 ${\mu}M$ FK506 to Hep3B cells led to cell death accompanied by a decrease in cell viability and an increase in LDH, ROS and [$Ca^{2+}$]i. FK506 induced an increase in activity of Bax and JNK protein but inhibited the activity of Bcl-2 protein. Treatment of dexamethsone, per se, had no effects on cell viability, LDH and ROS. However, co-treatment of FK506 and dexamethasone diminished the FK506-induced LDH release, ROS generation and JNK activation. These results demonstrate that FK506 has antitumor effect in Hep3B cells but the combination of FK506 and dexamethasone antagonizes the FK506-induced antitumor effects.

• The Korea Journal of Herbology
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• v.22 no.2
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• pp.147-153
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• 2007

Objectives : Sophora flavescens (SF) is widely used in traditional herbal medicine in Korea and is well recognized for its anti-inflammatory effect. However, its effect on Tumornecrosis factor alpha (Tnf) production in BV2 microglial cell is not yet known. Methods : We investigated the effect of SF on the production and expression of Tnf, a well known inflammatory mediator, in lipopolysaccaride (LPS)-activated BV2 microglial cells. Results : The LPS-induced Tnf production was markedly reduced by treatment with SF (50 ${\mu}g/ml$). In reverse transcription polymerase chain reaction (RT-PCR) analysis, SF suppressed the LPS activated expression of Tnf mRNA. In addition, Western blot analysis confirmed that SF suppressed the expression of Tnf. Sophora flavescens also inhibited the LPS-induced phosphylation of extracellular signal-regulated kinases (ERK), which mediate the Tnfproduction signaling pathway whereas LPS-induced phosphylation of p38 mitogen activated protein kinase (p38 MAPK), and c-Jun NH2-terminal kinases (JNK) was not inhibited by SF, which implies that SF suppresses LPS-induced Tnf production via the ERK mediated pathway. Conclusion : Taken together, these findings indicated that SF inhibits LPS-induce Tnf production, and that this inhibitory effect is mediated via the ERK pathway.

• Food Science of Animal Resources
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• v.41 no.5
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• pp.749-762
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• 2021

Colostrum, which contains various immune and growth factors, aids wound healing by promoting keratinocyte proliferation. Aquaporins (AQPs) are small, hydrophobic membrane proteins that regulate cellular water retention. However, few studies have examined the effect of processed colostrum whey on AQP-3 expression in human skin cells. Here, we investigated the effect of milk, colostrum, fermented milk, and fermented colostrum whey on AQP-3 expression in keratinocyte HaCaT cells. Concentrations of 100-400 ㎍/mL of fermented colostrum whey were found to induce HaCaT cell proliferation. AQP-3 was found to be expressed exclusively in HaCaT cells. AQP-3 expression was significantly increased in 100 ㎍/mL fermented colostrum whey-treated cells compared with that in controls. Moreover, fermented colostrum increased p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) phosphorylation, but not ERK1/2 phosphorylation. Thus, our results suggest that fermented colostrum whey increased AQP-3 expression in, and the proliferation of, keratinocytes via JNK and p38 MAPK activation.

• Nutrition Research and Practice
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• v.13 no.4
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• pp.279-285
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• 2019

BACKGROUND/OBJECTIVES: Excessive production of reactive oxygen species (ROS) such as hydroxyl (${\cdot}OH$), nitric oxide (NO), and hydrogen peroxide ($H_2O_2$) is reported to induce oxidative stress. ROS generated by oxidative stress can potentially damage glial cells in the nervous system. Cordyceps militaris (CM), a kind of natural herb widely found in East Asia. In this study, we investigated the free radical scavenging activity of the CM extract and its neuroprotective effects in $H_2O_2$-induced C6 glial cells. MATERIALS/METHODS: The ethanol extract of CM ($100-1,000{\mu}g/mL$) was used to measure DPPH, ${\cdot}OH$, and NO radical scavenging activities. In addition, hydrogen peroxide ($H_2O_2$)-induced C6 glial cells were treated with CM at $0.5-2.5{\mu}g/mL$ for measurement of cell viability, ROS production, and protein expression resulting from oxidative stress. RESULTS: The CM extract showed high scavenging activities against DPPH, ${\cdot}OH$, and NO radicals at concentration of $1,000{\mu}g/mL$. Treatment of CM with $H_2O_2$-induced oxidative stress in C6 glial cells significantly increased cell viability, and decreased ROS production. Cyclooxygenase-2 and inducible nitric oxide synthase protein expression was down-regulated in CM-treated groups. In addition, the protein expression level of phospho-p38 mitogen-activated protein kinase (p-p38 MAPK), phospho-c-Jun N-terminal kinase (p-JNK), and phospho-extracellular regulated protein kinases (p-ERK) in $H_2O_2$-induced C6 glial cells was down-regulated upon CM administration. CONCLUSION: CM exhibited radical scavenging activity and protective effect against $H_2O_2$ as indicated by the increased cell viability, decreased ROS production, down-regulation of inflammation-related proteins as well as p-p38, p-JNK, and p-ERK protein levels. Therefore, we suggest that CM could play the protective role from oxidative stress in glial cells.