• Bulletin of the Korean Chemical Society
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• v.31 no.4
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• pp.989-998
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• 2010

The titled dye of DBPI gives amplified spontaneous emission (ASE) with maximum at 580 nm upon pumping by nitrogen laser (${\lambda}_{ex}\;=\;337.1\;nm$). The ground state absorption cross section (${\sigma}_A$) and emission cross section (${\sigma}_E$) as well as effective emission cross section(${\sigma}^*_E$) have been determined. The electronic absorption spectra of DBPI were measured in ethanol and tetrahydrofuran at room and low temperature. DBPI displays molecular aggregation in water. The photochemical reactivity of DBPI was also studied in carbon tetrachloride upon irradiation with 525 nm light. The electrochemical investigation of DBPI dye has been carried out using cyclic voltammetry and convolution deconvolution voltammetry combined with digital simulation technique at a platinum electrode in 0.1 mol/L tetrabutyl ammonium perchlorate (TBAP) in two different solvents acetonitrile ($CH_3CN$) and dimethylformamide (DMF). The species were reduced via consumption of two sequential electrons to form radical anion and dianion (EE mechanism). In switching the potential to positive direction, the compound was oxidized by loss of two sequential electrons, which were followed by a fast dimerization and/or aggregation process i.e $EC_{dim1}EC_{dim2}$ mechanism. The electrode reaction pathway and the chemical and electrochemical parameters of the investigated compound were determined using cyclic and convolutive voltammetry. The extracted electrochemical parameters were verified and confirmed via digital simulation method.

• BMB Reports
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• v.38 no.3
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• pp.360-365
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• 2005

Membrane inositol glycerophospholipid (IGP) is metabolized to phosphatidylinositol-4-phosphate (PIP), phosphatidylinositol-4, 5-bisphosphate ($PIP_2$), and inositol triphosphate ($IP_3$) in signaling transduction. This study was carried out to determine the subclasses of IGP involved in signaling pathway. The acyl chain moieties of the phospholipids are easily modulated by dietary fatty acids. We analyzed acyl chain composition of IGP 3-subclasses, PIP and $PIP_2$ from rat brain after feeding sunflower seed oil enriched with linoleic acid or fish oil high in eicosapentaenoic acid and docosahexaenoic acid. Long chain polyunsaturated fatty acids (LCPUFA) as eicosapentaenoic acid and docosahexaenoic acid were not incorporated into ether-linked IGP (alkenylacylglycerophosphoinositol and alkylacyl-glycerophosphoinositol), PIP and $PIP_2$, while diacyl-glycerophosphoinositol (GPI) contained high LCPUFA. These results suggest that PIP might be phosphorylated from only the ether-linked IGP (alkenylacyl- and alkylacyl species) but not from diacyl subclass for signals to intracellular responses in the plasma membrane of rat brain.

• Biomedical Science Letters
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• v.15 no.1
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• pp.61-66
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• 2009

Leflunomide is an immunomodulatory agent used for the treatment of rheumatoid arthritis (RA). Leflunomide known as a regulator of iNOS synthesis which largely decreases NO production in diverse cell type. However, the effect of leflunomide on chondrocyte is still poorly understood. In our previous studies, we have shown that direct production of Nitric oxide (NO) by treating chondrocytes with NO donor, sodium nitroprusside (SNP), causes apoptosis via p38 mitogen-activated protein kinase in association with elevation of p53 protein level, caspase-3 activation. In this study, we characterized the molecular mechanism by which A77 1726 inhibit apoptosis. We found that A77 1726 inhibit NO-induced apoptosis as determined by MTT (Thiazolyl Blue Tetrazolium Bromide) assay and DNA fragmentation. The inhibition of apoptosis by A77 1726 was accompanied by increased PI-3 kinase and AKT activities. So, inhibition of phosphatidylinositol (PI)-3kinase with LY294002 rescued apoptosis. Triciribine, the specific inhibitor of AKT, also abolished anti-apoptotic effect. Our results indicate that A77 1726, the active metabolite of leflunomide, mediates NO-induced apoptosis in chondrocytes by modulating up-regulation of PI-3 kinase and AKT.

• BMB Reports
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• v.37 no.4
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• pp.445-453
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• 2004

We identified apoptosis as being a significant mechanism of toxicity following the exposure of HeLa cell cultures to abrin holotoxin, which is in addition to its inhibition of protein biosynthesis by N-glycosidase activity. The treatment of HeLa cell cultures with abrin resulted in apoptotic cell death, as characterized by morphological and biochemical changes, i.e., cell shrinkage, internucleosomal DNA fragmentation, the occurrence of hypodiploid DNA, chromatin condensation, nuclear breakdown, DNA single strand breaks by TUNEL assay, and phosphatidylserine (PS) externalization. This apoptotic cell death was accompanied by caspase-9 and caspase-3 activation, as indicated by the cleavage of caspase substrates, which was preceded by mitochondrial cytochrome c release. The broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), prevented abrin-triggered caspase activation and partially abolished apoptotic cell death, but did not affect mitochondrial cytochrome c release. These results suggest that the release of mitochondrial cytochrome c, and the sequential caspase-9 and caspase-3 activations are important events in the signal transduction pathway of abrin-induced apoptotic cell death in the HeLa cell line.

• BMB Reports
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• v.44 no.6
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• pp.399-404
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• 2011

In this study, powder of Orostachys japonicus A. Berger (O. japonicus) was extracted with 95% ethyl alcohol and fractionated using a series of organic solvents, including n-hexane (hexane), dichloromethane (DCM), ethylacetate (EtOAc), n-butanol (BuOH), and water ($H_2O$). We investigated the anti-inflammatory effects of these O. japonicus extracts on lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Their effects on the expression of inflammatory mediators and transcription factors were analyzed by Western blotting. DCM fraction significantly inhibited formation of reactive oxygen species (ROS) as well as nitric oxide (NO) in LPS-stimulated RAW 264.7 cells. Phosphorylation of the pro-inflammatory transcription factor complex nuclear factor-kappa B (NF-${\kappa}$B) p65 and expression of inducible nitric oxide synthase (iNOS), one of its downstream proteins, were also suppressed by DCM fraction. These effects were regulated by upsteam proteins in the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathways. Taken together, our data suggest that O. japonicus could be used as a potential source for anti-inflammatory agents.

• BMB Reports
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• v.48 no.10
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• pp.539-540
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• 2015

It has been proposed that the selective elimination of cancer stem cells (CSCs) using targeted therapy could greatly reduce tumor growth, recurrence, and metastasis. To develop effective therapeutic targets for CSC elimination, we aimed to define the properties of CSC mitochondria, and identify CSC-mitochondria-specific targets in colon cancer. We found that colon CSCs utilize mitochondrial oxidative phosphorylation (OXPHOS) to produce ATP. We also found that forkhead box protein 1 (FOXM1)-induced peroxiredoxin 3 (PRDX3) maintains the mitochondrial function, and the FOXM1/PRDX3 mitochondrial pathway maintains survival of colon CSCs. Furthermore, FOXM1 induces CD133 (PROM1/prominin 1) expression, which maintains the stemness of colon CSCs. Together, our findings indicate that FOXM1, PRDX3, and CD133 are potential therapeutic targets for the elimination of CSCs in colon cancer.

• BMB Reports
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• v.46 no.7
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• pp.352-357
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• 2013

Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-${\alpha}$-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-${\alpha}$-induced HASMCs and reduced NF-${\kappa}B$ activation. Furthermore, P. vulgaris extract suppressed TNF-${\alpha}$-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses anti-inflammatory properties and can regulate TNF-${\alpha}$-induced expression of adhesion molecules by inhibiting the p38 MAPK/ERK signaling pathway.

• BMB Reports
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• v.51 no.3
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• pp.126-133
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• 2018

Hippo signaling plays critical roles in regulation of tissue homeostasis, organ size, and tumorigenesis by inhibiting YES-associated protein (YAP) and PDZ-binding protein TAZ through MST1/2 and LATS1/2 pathway. It is also engaged in cross-talk with various other signaling pathways, including WNT, BMPs, Notch, GPCRs, and Hedgehog to further modulate activities of YAP/TAZ. Because YAP and TAZ are transcriptional coactivators that lack DNA-binding activity, both proteins must interact with DNA-binding transcription factors to regulate target gene's expression. To activate target genes involved in cell proliferation, TEAD family members are major DNA-binding partners of YAP/TAZ. Accordingly, YAP/TAZ were originally classified as oncogenes. However, YAP might also play tumor-suppressing role. For example, YAP can bind to DNA-binding tumor suppressors including RUNXs and p73. Thus, YAP might act either as an oncogene or tumor suppressor depending on its binding partners. Here, we summarize roles of YAP depending on its DNA-binding partners and discuss context-dependent functions of YAP/TAZ.

• International Journal of Oral Biology
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• v.40 no.2
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• pp.85-91
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• 2015

Quercetin is a natural flavonoid phytochemical that is extracted from various plants. Having an advantages due to its varied biological properties, such as anti-inflammatory, anti-viral, anti-oxidant, and anti-cancer effects, quercetin is used to treat many diseases. Recently, it has been reported that autophagy inhibition may play a key role in anti-cancer therapy. Therefore, in this study, we investigated the molecular mechanisms and anti-cancer effects of quercetin in human osteosarcoma cells via autophagy inhibition. We ascertained that quercetin inhibited cell proliferation and induced cell death, these process is demonstrated that apoptosis via the mitochondrial pathway and the caspase cascade. Quercetin also induced autophagy which was inhibited by 3-MA, autophagy inhibitor and the blockade of autophagy promoted the quercetin-induced apoptosis, confirming that autophagy is a pro-survival process. Thus, these findings demonstrate that quercetin is an effective anti-cancer agent, and the combination of quercetin and an autophagy inhibitor should enhance the effect of anti-cancer therapy.

• Journal of Ginseng Research
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• v.21 no.1
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• pp.1-12
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• 1997

Ginseng, the root of Panax ginseng C.A. Meyer, is well-known oriental herbal medicine. The number of paper reporting the effects on its physiological, pharmacological, and behavioral effects has been increased every year, since ginsenosides isolated from ginseng are known to be biologically active components. This brief review summarizes some of new findings from recently published papers on ginsenosides or ginseng saponins. Therefore, this paper includes the various effects of ginsenosides on neuronal cell growths, on behavior of experimental animals, on enzyme activities, on the release and uptake of neurotransmitters, on neuronal cell excitability, on the motility of intestine, on antitumor activity, on cardiovascular system and metabolism. In spite of various effects of ginsenosides on various cells or organs, it is still to date impossible for one to clearly explain the exact mechanism on the action of ginsenosides. However, in this article I will discuss several papers providing possible explanations on the physiological and pharmacological actions including signal transudation pathway of ginsenosides. The elucidation of the exact mechanism of ginsenosides on cellular or molecular level will not only give us a chance to explain why people have used ginseng as an elixir of life for several thousands of year but also give us a crucial chance to apply ginseng to modern medicine.