• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.117-123
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• 2005

A cumulative evidence indicates that consumption of tea catechin, flavan-3-ol derived from green tea leaves, lowers the risk of cardiovascular diseases. However, a precise mechanism for this cardiovascular action has not yet been fully understood. In the present study, we investigated the effects of different green tea catechins, such as epigallocatechin-3 gallate (EGCG), epigallocatechin (EGC), epicatechin-3 gallate (ECG), and epicatechin (EC), on angiotensin II (Ang II)-induced hypertrophy in primary cultured rat aortic vascular smooth muscle cell (VSMC). [$^3H$]-leucine incorporation was used to assess VSMC hypertrophy, protein kinase assay, and western blot analysis were used to assess mitogen-activated protein kinase (MAPK) activity, and RT-PCR was used to assess c-jun or c-fos transcription. Ang II increased [$^3H$]-leucine incorporation into VSMC. However, EGCG and ECG, but not EGC or EC, inhibited [$^3H$]-leucine incorporation increased by Ang II. Ang II increased phosphorylation of c-Jun, extracellular-signal regulated kinase (ERK) 1/2 and p38 MAPK in VSMC, however, EGCG and ECG , but not EGC or EC, attenuated c-Jun phosphorylation increased by Ang II. ERK 1/2 and p38 MAPK phosphorylation induced by Ang II were not affected by any catechins. Ang II increased c-jun and c-fos mRNA expression in VSMC, however, EGCG inhibited c-jun but not c-fos mRNA expression induced by Ang II. ECG, EGC and EC did not affect c-jun or c-fos mRNA expression induced by Ang II. Our findings indicate that the galloyl group in the position 3 of the catechin structure of EGCG or ECG is essential for inhibiting VSMC hypertrophy induced by Ang II via the specific inhibition of JNK signaling pathway, which may explain the beneficial effects of green tea catechin on the pathogenesis of cardiovascular diseases observed in several epidemiological studies.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.69-74
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• 1999

Both direct and indirect environmental stress to brain were increase the expression of transcription factor c-fos in various populations of neurons. In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsion within 10 min increased the level of c-fos mRNA and protein in forebrain areas. In situ hybridization using $[^{35}S]UTP-labeled$ antisense c-fos, cRNA increased c-fos mRNA levels though hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr. In parallel with the mRNA expression, c-FOS protein immunoreactivity was also observed in the same forebrain areas. In contrast to the seizure activity and widespread neuronal degeneration following a kainate treatment, injections of lidocaine did not produce neuronal death within 3 days. The present study indicates that lidocaine induces convulsion and c-fos expression without causing neurotoxicity.

• BMB Reports
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• v.43 no.1
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• pp.57-61
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• 2010

Activator protein-1 can induce either cell survival or death, which is controlled by opposing effects of different Jun members. It is generally accepted that c-Jun is pro-apoptotic, but that JunD is anti-apoptotic in stress-exposed cells. Additionally, although there are reports suggesting that JunB plays a protective role, its role in stress-induced apoptosis remains unclear. Here, we investigated the role of JunB in $H_2O_2$-induced cell death using cells that over-expressed the protein or were transfected with si-JunB. Inhibition of JunB expression accelerated $H_2O_2$-mediated loss of mitochondrial membrane potential (MMP) and cytotoxicity. Conversely, over-expression of JunB protein led to significant inhibition of the MMP loss and cell death. The increase in JunB expression also attenuated nuclear relocation of apoptosis-inducing factor and mitochondrial Bcl-2 reduction that occurred following $H_2O_2$ exposure. These results suggest that JunB can signal survival against oxidant-mediated cell death by suppressing mitochondrial stress.

• Journal of Digital Convergence
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• v.13 no.8
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• pp.503-514
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• 2015

The effects of Flavonol contents from Ginkgo biloba leaf on anti-atopy activity have not rarely been verified. This study is to investigate the effects of flavonol on Th2 cytokine production in MC/9 mast cells. For this, flavonol was analyzed by ELISA and Real-time PCR. Analysis results showed that flavonol significantly suppressed production of Th2 cytokines(IL-13, MIP-1a) in a dose dependent manner. The mRNA expression of IL-4, IL-5, IL-13, TNF-a were effectively restrained by Flavonol at the concentration 25,50,$100{\mu}g/m{\ell}$. And decrease of expression of NFAT-1, c-jun protein was confirmed by western blot analysis. These results indicate that flavonol has effects of decreasing the Th2 cytokine production in the MC/9 mast cell causing inhibition of transcription factors such as NFAT-1, c-jun. Thus, we would like to brief that flavonol may have the applicability as therapeutic agent for atopic dermatitis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.4
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• pp.411-416
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• 2014

Simple formulas (單方) of muscle section in Donguibogam (東醫寶鑑) have long been prescribed for strengthening muscle and/or prevention of age-related muscle loss. However, biological activity and mechanisms by which they influence myoblast differentiation have not been studied. Therefore, in this study, we evaluated the effects of 14 simple formulas on myoblast differentiation in C2C12 myoblast cells under non-cytotoxic ($0.5mg/m{\ell}$) conditions. C2C12 cells were treated with water extracts of simple formulas for 72 h, and RT-PCR was performed to determine the gene expression levels of myogenic regulatory factors (MRFs), including myoD, myogenin, MRF4, myf5, and insulin like growth factor-1 (IGF-1). Treatment with Colocasiae Rhizoma (CR), Pini Semen (PS), and Sesami Semen (SS) resulted in a significant increase in expression of myogenin in C2C12 cells. Treatment with Allii Macrostemi Bulbus (AM), Colocasiae Rhizoma (CR), and Pini Semen (PS) also resulted in increased expression of MRF4 in C2C12 cells. In addition, enhanced expression of IGF-1 was observed in treatment with Eucommiae cortex (EC), Dioscoreae Rhizoma (DR), Colocasiae Rhizoma (CR), Pini Semen (PS), and Sesami Semen (SS) in C2C12 cells. These results indicate that simple formulas of muscle section in Donguibogam could potentially enhance myoblast differentiation at least in part via increasing expression of myogenin, and/or MRF4 and/or IGF-1.

• The Journal of the Korean Society for Microbiology
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• v.35 no.4
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• pp.299-308
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• 2000

Recently developed cDNA microarray or DNA chip technology allows expression monitoring of expression of hundreds and thousands of genes simultaneously and provides a format for identifying genes as well as changes in their activity. In order to search for changes in gene expression after X irradiation in HL60 cells, cDNA microarray technique was done. In this study, expression of 588 human genes (including oncogenes, tumor suppressor genes, cell cycle regulator genes, intracellular signal transduction modulator genes, apoptosis related genes, transcription factor genes, growth factors and receptor genes, cytokine genes, etc) were analyzed. For cDNA microarray analysis mRNAs were extracted from control and 8 Gy-irradiated HL60 cells. As a result the changes in expression of several genes were observed. This alteration of gene expression was confirmed by reverse transcription-polymerase chain reaction. The expression of heat shock 60 KD protein, c-jun, erythroid differentiation factor, CPP32, myeloid cell nuclear differentiation antigen, MAP kinase-activated protein kinase, interleukin-8, monocyte chemotactic peptide 1 and RANTES genes was increased, but the expression of p55CDC gene was decreased after X irradiation.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.42 no.4
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• pp.393-401
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• 2016

Ultraviolet (UV) irradiation from the sun is the primary environmental factor that causes skin damages including skin cancer and premature skin aging. Because, even the most powerful sunscreen can't always afford enough protection, it is necessary to enhance the defensive power of skin against UV. Recently, constitutive photomorphogenic protein-1 (COP1) has shown to contribute to the regulation of UVB response of keratinocytes. In this study, we represent that COP1 and its associated protein, de-etiolated 1 (DET1), might participate in photoaging process in human skin as Arabidopsis COP1 does sun-protective function in plants. After UVB irradiation, the decrease of COP1 and DET1 mRNA expression was followed by the increase of c-Jun total protein. Moreover, transfection with DNA vectors expressing COP1 and DET1 down-regulated the c-Jun total protein. We found that Zanthoxylum piperitum extract (ZE) up-regulated the expression of COP1 and DET1 on human keratinocytes, and inhibited the expression of MMP1 which is one of the genes regulated by c-Jun signal. In addition, ZE has been reported to stimulate PPAR-${\alpha}$ and strengthen the skin barrier. We found that ZE decreased the UVB-induced IL-6 and IL-8 in NHEK cells. In human study, ZE protected skin against UV-B induced erythema and erythema-induced pigmentation. These results indicate that ZE could be useful for the protection against the adverse effects of UV irradiation through various mechanisms.

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.342.2-342
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• 1995

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.305.1-305
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• 1995

No Abstract, See Full Text

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.3
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• pp.330-337
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• 2012

This study was performed to assess the Effect of SCF(Schisandrae Chinensis Fructus) on Keratinocyte Damage by UV irradiation. The effect of SCF were determined in UV irradiated HaCaT. We measured LDH release and NO release from HaCaT to elucidate the effect of SCF. And iNOS, TNF-${\alpha}$, COX-2, Bax, Bcl-2, Bcl-xL, c-jun, c-fos gene expression were determined in HaCat using real time PCR method. The results are as follows. SCF inhibited LDH-release, NO production in UV irradiated HaCaT. SCF increased the gene expression Bax, Bcl-2 and Bcl-xL protein in UV irradiated HaCaT. SCF suppressed the gene expression TNF-${\alpha}$ in UV irradiated HaCaT. SCF suppressed the gene expression iNOS, c-fos, and c-jun in UV irradiated HaCaT. SCF not affected the suppression of the gene expression COX-2 in UV irradiated HaCaT. The study showed SCF inhibited the cell damage in UV irradiated HaCaT.