• Korean Journal of Plant Resources
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• v.10 no.2
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• pp.183-187
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• 1997

This study was carried out to find the growth characteristics and content of sarsasapogenin in different plant parts of Anemarrhena asphodeloides Bunge. Five native-cultivars were collected and evaluated for several agronomic traits. The collected native-cultivars were classified into two seed-attached peduncle and vegetative propagation types. Seed-attached peduncle lines were predominance of growth traits than vegetative propagation. For the content of sarsasapogenin in each part was investigated, BuOH extarct of 'timo' was developed on silica gel 60G plate using elution solvent($CHC1_2$: Methyl ethyl Ketone : EtOH = 11 : 2 : 0.5). The developed plate were examined using Dual Wavelength Zig - Zag using. Content of sarsasapogenin in main root and lateral root were respectively 1.67mg/g and 1.31mg/g.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.8
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• pp.3509-3515
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• 2015

Background: Diallyl disulfide (DADS) may exert potent anticancer action both in vitro and in vivo. Although its effects on cancer are significant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible links between DADS and pyruvate kinase (PKM2). Materials and Methods: $KG1{\alpha}$, a leukemia cell line highly expressing PKM2 was used with a cell counting kit (CCK)-8 and flow cytometry (FCM) to investigate the effects of DADS. Relationships between PKM2 and DADS associated with phosphorylation of EGFR, ERK1/2 and MEK, were assessed by western blot analysis. Results: In $KG1{\alpha}$ cells highly expressing PKM2, we found that DADS could affect proliferation, apoptosis and EGFR/ERK/PKM2 signaling pathways, abrogating EGF-induced nuclear accumulation of PKM2. Conclusions: These results suggested that DADS suppressed the proliferation of $KG1{\alpha}$ cells, providing evidence that its proapoptotic effects are mediated through the inhibition of EGFR/ERK/PKM2 signaling pathways.

• Archives of Pharmacal Research
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• v.27 no.3
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• pp.324-333
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• 2004

To determine whether Insulin-like growth factor (IGF-I) treatment represents a potential means of enhancing the survival of cardiac muscle cells from adriamycin (ADR)-induced cell death, the present study examined the ability of IGF-I to prevent cell death. The study was performed utilising the embryonic, rat, cardiac muscle cell line, H9C2. Incubating cardiac muscle cells in the presence of adriamycin increased cell death, as determined by MTT assay and annexin V-positive cell number. The addition of 100 ng/mL IGF-I, in the presence of adriamycin, decreased apoptosis. The effect of IGF-I on phosphorylation of PI, a substrate of phosphatidylinositol 3-kinase (PI 3-kinase) or protein kinase B (AKT), was also examined in H9C2 cardiac muscle cells. IGF-I increased the phosphorylation of ERK 1 and 2 and $PKC{\;}{\zeta}{\;}kinase$. The use of inhibitors of PI 3-kinase (LY 294002), in the cell death assay, demonstrated partial abrogation of the protective effect of IGF-I. The MEK1 inhibitor-PD098059 and the PKC inhibitor-chelerythrine exhibited no effect on IGF-1-induced cell protection. In the regulatory subunit of PI3K-p85- dominant, negative plasmid-transfected cells, the IGF-1-induced protective effect was reversed. This data demonstrates that IGF-I protects cardiac muscle cells from ADR-induced cell death. Although IGF-I activates several signaling pathways that contribute to its protective effect in other cell types, only activation of PI 3-kinase contributes to this effect in H9C2 cardiac muscle cells.

• Molecules and Cells
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• v.21 no.2
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• pp.237-243
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• 2006

Brain-derived neurotrophic factor (BDNF) is a neuromodulator of nociceptive responses in the dorsal root ganglia (DRG) and spinal cord. BDNF synthesis increases in response to nerve growth factor (NGF) in trkA-expressing small and medium-sized DRG neurons after inflammation. Previously we demonstrated differential activation of multiple BDNF promoters in the DRG following peripheral nerve injury and inflammation. Using reporter constructs containing individual promoter regions, we investigated the effect of NGF on the multiple BDNF promoters, and the signaling pathway by which NGF activates these promoters in PC12 cells. Although all the promoters were activated 2.4-7.1-fold by NGF treatment, promoter IV gave the greatest induction. The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294003, protein kinase A (PKA) inhibitor, H89, and protein kinase C (PKC) inhibitor, chelerythrine, had no effect on activation of promoter IV by NGF. However, activation was completely abolished by the MAPK kinase (MEK) inhibitors, U0126 and PD98059. In addition, these inhibitors blocked NGF-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2. Taken together, these results suggest that the ERK1/2 pathway activates BDNF promoter IV in response to NGF independently of NGF-activated signaling pathways involving PKA and PKC.

• Textile Coloration and Finishing
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• v.24 no.1
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• pp.79-90
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• 2012

This study surveys the characteristics of the PU/MWNT foaming film according to foaming conditions. For this purpose, firstly, 16 kinds of PU/MWNT forming films were prepared with 4 kinds of dispersion solutions (IPA/MWNT, DMF/MWNT, MEK/MWNT, and Toluene/MWNT) and 4 kinds of blowing agents (organic I, organic II, capsule, and inorganic). The electrical resistivity of these PU/MWNT foaming films according to the dispersion solutions and blowing agents were analysed and discussed with surface profile and cell morphology of measured by SEM. And secondly, 24 kinds of PU/MWNT foaming films were also prepared with 2 kinds of IPA dispersion solution contents and 3 kinds of blowing agents with variation of the blowing temperatures and film thickness. The physical properties of the PU/MWNT foaming films such as electrical resistivity (surface and volume) and triboelectricity with cell morphology were measured and discused through the quantities of IPA, blowing agent added and also physical conditions(temperature, thickness so on) for establishing optimum foaming conditions with good electrostatic dissipation.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.3
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• pp.225-234
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• 2018

Adenosine is a naturally occurring breakdown product of adenosine triphosphate and plays an important role in different physiological and pathological conditions. Adenosine also serves as an important trigger in ischemic and remote preconditioning and its release may impart cardioprotection. Exogenous administration of adenosine in the form of adenosine preconditioning may also protect heart from ischemia-reperfusion injury. Endogenous release of adenosine during ischemic/remote preconditioning or exogenous adenosine during pharmacological preconditioning activates adenosine receptors to activate plethora of mechanisms, which either independently or in association with one another may confer cardioprotection during ischemia-reperfusion injury. These mechanisms include activation of $K_{ATP}$ channels, an increase in the levels of antioxidant enzymes, functional interaction with opioid receptors; increase in nitric oxide production; decrease in inflammation; activation of transient receptor potential vanilloid (TRPV) channels; activation of kinases such as protein kinase B (Akt), protein kinase C, tyrosine kinase, mitogen activated protein (MAP) kinases such as ERK 1/2, p38 MAP kinases and MAP kinase kinase (MEK 1) MMP. The present review discusses the role and mechanisms involved in adenosine preconditioning-induced cardioprotection.

• 한국생물공학회:학술대회논문집
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• 2005.04a
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• pp.247-251
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• 2005

This research was performed for developing of biological treatment process of odor gas such as MEK, $H_{2}S$, and toluene, which is generated from the food waste recycling process. To establish the operational conditions of odor gas removal by small-scale biofiltration equipment, it was continuously operated by using toluene as a treating odor object. When the odor treating microorganisms were adhered to fibril form biofilter, high removal efficiency over 93% was obtained by biofilm formation. At 400 ppm of inlet odor gas concentration and 10 sec of retention time, the removal efficiency was 76% and 93% in 1st stage reactor and 2nd stage reactor, respectively. However, the removal efficiency remained over 97% at the operational conditions above 15 sec of retention time.

• Proceedings of the Korean Society of Dyers and Finishers Conference
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• 2012.03a
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• pp.105-105
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• 2012

기능성 아웃도어 제품을 제조하기 위해서 사용되어지는 멤브레인은 크게 미세다공형과 친수무공형으로 구분할 수 있다. 최근에는 소비자들이 기능성 아웃도어에 쾌적성을 요구하고 있으며, 그 측면에서 본다면 미세다공형 멤브레인이 친수무공형보다 유리하다. 기존의 미세다공형 멤브레인은 고가이며, casting이 불가능한 단점을 가지고 있다. 본 연구에서는 분자구조 및 유화제 첨가에 따른 casting이 가능한 미세다공형 폴리우레탄 멤브레인의 특성에 대하여 연구하였다. Casting용 미세다공형 폴리우레탄은 soft segment와 hard segment의 비가 1/2일 때, 그리고 사용되는 용제가 MEK 단독일 때 안정적인 반응성과 이상적인 필름의 물성을 보이는 것을 확인 하였으며, 수지에 첨가되는 분산유화제의 양이 10%이상일 때 상분리 현상이 발생하지 않음을 확인 할 수 있었다. 개발된 수지의 적용성을 평가한 결과, J-knife를 이용하여 knife over roll 방식으로 25~35$g/m^2$ (dry add on)를 도포하여 $80/120/140^{\circ}C{\times}10m/min$의 다단건조 공정으로 진행했을 때 최적의 물성을 얻을 수 있었다.

• Journal of Microbiology and Biotechnology
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• v.30 no.1
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• pp.31-37
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• 2020

We previously identified a new heparinase inhibitor fungal metabolite, named CRM646-A, which showed inhibition of heparinase and telomerase activities in an in vitro enzyme assay and antimetastatic activity in a cell-based assay. In this study, we elucidated the mechanism by which CRM646-A rapidly induced nucleus condensation, plasma membrane disruption and morphological changes by increasing intracellular Ca²⁺ levels. Furthermore, PD98059, a mitogen-activated protein kinase (MEK) inhibitor, inhibited CRM646-A-induced nucleus condensation through ERK1/2 activation in rat 3Y1 fibroblast cells. We identified CRM646-A as a Ca²⁺ ionophore-like agent with a distinctly different chemical structure from that of previously reported Ca²⁺ ionophores. These results indicate that CRM646-A has the potential to be used as a new and effective antimetastatic drug.

• Tuberculosis and Respiratory Diseases
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• v.82 no.1
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• pp.42-52
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• 2019

Background: Transforming growth factor ${\beta}$ (TGF-${\beta}$), retinoic acid (RA), p38 mitogen-activated protein kinase (MAPK), and MEK signaling play critical roles in cell differentiation, proliferation, and apoptosis. We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-${\beta}1$. Methods: A549 epithelial cells and CCD-11Lu fibroblasts were incubated and stimulated with or without all-trans RA (ATRA) and TGF-${\beta}1$ and with MAPK or MEK inhibitors. The levels of p-Smad2/3 were analyzed by western blotting. For animal models, we studied three experimental mouse groups: control, bleomycin, and bleomycin+ATRA group. Changes in histopathology, lung injury score, and levels of TGF-${\beta}1$ and Smad3 were evaluated at 1 and 3 weeks. Results: When A549 cells were pre-stimulated with TGF-${\beta}1$ prior to RA treatment, RA completely inhibited the p-Smad2/3. However, when A549 cells were pre-treated with RA prior to TGF-${\beta}1$ stimulation, RA did not completely suppress the p-Smad2/3. When A549 cells were pre-treated with MAPK inhibitor, TGF-${\beta}1$ failed to phosphorylate Smad2/3. In fibroblasts, p38 MAPK inhibitor suppressed TGF-${\beta}1$-induced p-Smad2. In a bleomycin-induced lung injury mouse model, RA decreased the expression of TGF-${\beta}1$ and Smad3 at 1 and 3 weeks. Conclusion: RA had inhibitory effects on the phosphorylation of Smad induced by TGF-${\beta}1$ in vitro, and RA also decreased the expression of TGF-${\beta}1$ at 1 and 3 weeks in vivo. Furthermore, pre-treatment with a MAPK inhibitor showed a preventative effect on TGF-${\beta}1$/Smad phosphorylation in epithelial cells. As a result, a combination of RA and MAPK inhibitors may suppress the TGF-${\beta}1$-induced lung injury and fibrosis.