• The Korea Journal of Herbology
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• v.27 no.4
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• pp.73-80
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• 2012

Objectives : Under normal condition melanin protects the skin from extracellular stimuli including ultraviolet (UV)-induced oxidative skin damages, but excess production and accumulation of melanin can induce hyperpigmentation causing esthetic problems. Therefore, in this study we tried to search for natural skin whitening materials from marine natural resources. Methods : Water and ethanol extracts of marine natural resources were prepared from Porphyra thalli (PT), Laminariae thallus (LT), Ostreae concha (OC), Sargassum thallus (ST), Undaria thallus (UT), Codium thalli (CT), Enteromorpha thalli (ET), Syngnathoides biaculeatus (SB), and Hippocampus coronatus (Hc). Their effects against UVB and ${\alpha}$-melanocyte stimulating hormone (${\alpha}$-MSH)-induced melanogenesis were investigated based on melanin formation in B16 mouse melanoma cells. The mRNA and protein expression of enzymes involved in the melanogenic process were further examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. Results : Water extract of Ostreae concha (OCW/E) effectively inhibited UVB and ${\alpha}$-MSH-induced melanin production in B16 melanocytes, which seemed to be mediated by inhibition of mRNA expression of tyrosinase and tyrosinase-related protein 1 (TRP-1). In another experiment, ethanol extracts from Porphyra thalli (PTE/E), Laminariae thallus (LTE/E), Sargassum thallus (STE/E), Undaria thallus (UTE/E), Codium thalli (CTE/E), Syngnathoides biaculeatus (SBE/E), and Hippocampus coronatus (HcE/E) significantly suppressed UVB and ${\alpha}$-MSH-induced melanin formation. Furthermore, ethylacetate fraction isolated form LTE/E (LTE/EEt) decreased UVB and ${\alpha}$-MSH-elevated extracellular melanin levels via inhibition of tyrosinase protein expression. Conclutions : These results suggest that marine natural resources such as Porphyra thalli, Laminariae thallus, Ostreae concha, Sargassum thallus, Undaria thallus, Codium thalli, Syngnathoides biaculeatus and Hippocampus coronatus have anti-melanogenic effects, thereby exhibiting high potentials to be utilized as one of the ingredients for the development of new whitening functional cosmetics.

• Biomolecules & Therapeutics
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• v.24 no.2
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• pp.163-170
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• 2016

We examined whether apigenin affects the gene expression, secretion and activity of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as in vivo production of MMP-3 in the knee joint of rat to evaluate the potential chondroprotective effects of apigenin. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcription - polymerase chain reaction (RT-PCR) was used to measure interleukin-$1{\beta}$ (IL-$1{\beta}$)-induced expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), and ADAMTS-5. In rabbit articular chondrocytes, the effects of apigenin on IL-$1{\beta}$-induced secretion and proteolytic activity of MMP-3 were investigated using western blot analysis and casein zymography, respectively. The effect of apigenin on MMP-3 protein production was also examined in vivo. In rabbit articular chondrocytes, apigenin inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5. Furthermore, apigenin inhibited the secretion and proteolytic activity of MMP-3 in vitro, and inhibited production of MMP-3 protein in vivo. These results suggest that apigenin can regulate the gene expression, secretion, and activity of MMP-3, by directly acting on articular chondrocytes.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.239-245
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• 2014

We investigated whether luteolin affects the gene expression, secretion and activity of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as production of MMP-3 in the rat knee to evaluate the potential chondroprotective effects of luteolin. Rabbit articular chondrocytes were cultured in a monolayer and IL-$1{\beta}$-induced gene expression levels of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), ADAMTS-5 and type II collagen were measured by reverse transcription - polymerase chain reaction (RT-PCR). Effects of luteolin on interleukin- $1{\beta}$ (IL-$1{\beta}$)-induced secretion and enzyme activity of MMP-3 in rabbit articular chondrocytes were investigated by western blot analysis and casein zymography, respectively. The effect of luteolin on MMP-3 protein production was also examined in vivo. The results were as follows: (1) luteolin inhibited the gene expression levels of MMP-3, MMP-1, MMP-13, ADAMTS-4 and ADAMTS-5. However, it increased the gene expression level of collagen in rabbit articular chondrocytes; (2) luteolin inhibited the secretion and activity of MMP-3; (3) luteolin inhibited in vivo production of MMP-3 protein. These results suggest that luteolin can regulate the gene expression, secretion and activity of MMP-3, by directly acting on articular chondrocytes.

• Journal of Ginseng Research
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• v.42 no.4
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• pp.419-428
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• 2018

Background: Despite the large number of studies on ginseng, pharmacological activities of ginseng seed oil (GSO) have not been established. GSO is rich in unsaturated fatty acids, mostly oleic and linoleic acids. Unsaturated fatty acids are known to exert a therapeutic effect in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the protective effect and underlying mechanisms of GSO against NAFLD using in vitro and in vivo models. Methods: In vitro lipid accumulation was induced by free fatty acid mixture in HepG2 cells and by 3 wk of high fat diet (HFD)-feeding in Sprague-Dawley rats prior to hepatocyte isolation. The effects of GSO against diet-induced hepatic steatosis were further examined in C57BL/6J mice fed a HFD for 12 wk. Results: Oil Red O staining and intracellular triglyceride levels showed marked accumulation of lipid droplets in both HepG2 cells and rat hepatocytes, and these were attenuated by GSO treatment. In HFD-fed mice, GSO improved HFD-induced dyslipidemia and hepatic insulin resistance. Increased hepatic lipid contents were observed in HFD-fed mice and it was lowered in GSO (500 mg/kg)-treated mice by 26.4% which was evident in histological analysis. Pathway analysis of hepatic global gene expression indicated that GSO increased the expression of genes associated with ${\beta}$-oxidation (Ppara, Ppargc1a, Sirt1, and Cpt1a) and decreased the expression of lipogenic genes (Srebf1 and Mlxipl), and these were confirmed with reverse transcription and quantitative polymerase-chain reaction. Conclusion: These findings suggest that GSO has a beneficial effect on NAFLD through the suppression of lipogenesis and stimulation of fatty acid degradation pathway.

• The Korea Journal of Herbology
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• v.37 no.1
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• pp.51-59
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• 2022

Objectives : The process through which mesenchymal cells condense and differentiate into chondrocytes to form new bone is known as endochondral bone formation. Chondrogenic differentiation and hypertrophy are essential steps in bone formation and are influenced by various factors. The stem bark and root bark of Eleutherococcus sessiliflorus (ES) have been widely used to treat growth retardation and arthritis in traditional Korean Medicine. In this study, we aimed to investigate the possible role of the stem bark of ES in the stimulation of chondrogenic differentiation in clonal murine chondrogenic ATDC5 cells. Methods : In ATDC5 cells treated with ES extract, cell viability and extracellular matrix production were determined using CCK-8 assay and Alcian blue staining, respectively, and alkaline phosphatase activity was measured. We also examined mRNA and protein expression levels of genes related to chondrogenic expression in ATDC5 cells using reverse transcription-polymerase chain reaction and western blot analyses. Results : ES extract increased the accumulation of Alcian blue-stained cartilage nodules and alkaline phosphatase activity in ATDC5 cells. It increased the mRNA expressions of chondrogenic markers including bone sialoprotein (BSP), cartilage collagens, Runt-related transcription factor-2 (RUNX-2), osteocalcin (OCN), β-catenin, and bone morphogenetic protein-2 (BMP-2), as well as the protein expressions of β-catenin, RUNX-2, BMP-2, and alkaline phosphatase (ALP). Conclusion : Taken together, these results suggest that ES extract exhibits a chondromodulating activity and therefore may be a possible agent for the treatment of bone growth disorders.

• Journal of Periodontal and Implant Science
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• v.24 no.3
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• pp.472-482
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• 1994

Cytokines expressed specifically in leukocytes subsets and in activated cells, which are involved in chemotaxis and activation of leukocytes, are recently defined as chemokines. Macrophage inflammatory $protein-1{\alpha}(MIP-1{\alpha})$ and $MIP-1{\beta}$ are members of C-C chemokine subfamily which produces wide immunomodulatory, proinflammatory, and hematopoietic modulatory actions. We have studied their gene expression by using Northern blot analysis in various blood cells such as cytolytic T lymphocyte(CTL), helper T lymphocyte(HTL), macrophage, and B lymphocyte. Resting CTL line CTLL-R8 expressed $MIP-1{\alpha}$ mRNA which was downregulated by ConA stimulation. Both of resting and ConA stimulated HTL line Hut78 and Jurkat did not express $MIP-1{\alpha}$ mRNA. There was detectable $MIP-1{\alpha}$ transcript in HTL hybridoma 2B4.11 which was a little upstimulated by ConA stimulation. B cell line 230, and macrophage cell line RAW264.7 and WR19M.1 showed distinct $MIP-1{\alpha}$ message which were induced after LPS stimulation. Expression pattern of $MIP-1{\beta}$ in all cell lines or cell were almost identical to that of $MIP-1{\alpha}$. Also strategies employed to identify and characterize the biological functions was preceded by receptor cloning to trace the shorcut to the final goal of cytokine research. For the cloning of $MIP-1{\alpha}$ receptor(R), we used synthetic oligonucleotides of transmembrane(T) conserved sequences of already cloned human(h) IL-8-R, and performed reverse transcription-polymerase chain reaction(RT-PCR) amplification using murine(m) macrophage cell line mRNA. Among 5RT-PCR products, we isolated a homologous cDNA with hIL-8-R which were shown to be putative mIL-8-R cDNA.

• Biomolecules & Therapeutics
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• v.13 no.4
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• pp.240-245
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• 2005

An antimicrobial molecule was purified from centipede, Scolopendra subspinipes mutilans L. Koch, by reverse phase-HPLC. Its molecular weight was determined to be 1208.5493 by using matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry. Total amino acid composition analysis revealed that it consists of E, G, P, V, L, F, and W. It exhibited a broad antimicrobial spectrum against not only Gram-negative, but also Gram-positive bacteria. Furthermore, it was found to have an antimicrobial activity against vancomycin resistant enterococci (VRE). It may be a useful molecule for a new antibiotic development, especially against drug-resistant bacteria. We suggest that it may playa role in the defense system of this animal. This is the first report of a peptidic antimicrobial substance from centipede.

• Biomolecules & Therapeutics
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• v.16 no.3
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• pp.184-189
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• 2008

The proto-oncogene protein DEK has been implicated in various human disease including cancer. We have shown that DEK induces caspase-dependent apoptosis in Drosophila by regulating histone acetylation. Reverse transcription-polymerase chain reaction (RT-PCR) method based on annealing control primers was used to screen and identify differentially expressed genes (DEGs) in DEK overexpressed HeLa cells. Among the genes identified, clusterin and fibrillarin have major role in apoptosis pathway regulation. TFIIIC and RPS24 are implicated in HAT mediated transcriptional initiation and cololectal cancer, respectively. To further analyze DEK's role in apoptosis, multiplex PCR was performed. Caspase-3, -7, and -10 and proapoptotic gene bid were newly identified as possible target genes regulated by DEK expression.

• Biomolecules & Therapeutics
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• v.6 no.4
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• pp.417-422
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• 1998

Loxoprofen sodium (sodium 2-[4-(2-oxocyclopentylmethyl)phenyl] propionate dehydrate) is a nonsteroidal antiinflammatory drug of $\alpha$-phenyl propionic acid derivative. To test the bioequivalence of loxoprofen, the pharmacokinetic parameters of new preparation of loxoprofen, LENOX was compared with LOXONIN as a reference drug. Fourteen healthy volunteers were entered to the stydy (Yonsei University College of Medicine, Severance Hospital IRB approval No. 9608). They were administered 60 mg of loxoprofen in 2$\times$2 cross-over design. There was one week of drug-free interval between doses. The blood sample was taken on schedule up to 8 hours, and the plasma concentration loxoprofen was measured by reverse phase high-performance liquid chromatography (HPLC) with UV-detector. There were no significant difference between two preparations when AUC, Cmax, and Tmax were compared by ANOVA. The mean differences of AUC, Cmax, and Tmax were within 20% of the reference drug: the values were 2.22,5.61, and 12.50%, respectively. The confidence limits of AUC and Cmax but not Tmax satisfied the bioequivalence criteria. These results suggest that the tested LENOX is bioequivalent to the reference drug.

• Biomolecules & Therapeutics
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• v.25 no.6
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• pp.569-577
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• 2017

Sepsis is a syndrome characterized by systemic inflammatory responses to a severe infection. Acute hyper-inflammatory reactions in the acute phase of sepsis have been considered as a primary reason for organ dysfunction and mortality, and advances in emergency intervention and improved intensive care management have reduced mortalities in the early phase. However it has been recognized that increased deaths in the late phase still maintain sepsis mortality high worldwide. Patients recovered from early severe illness are unable to control immune system with sepsis-induced immunosuppression such as immunological tolerance, exhaustion and apoptosis, which make them vulnerable to nosocomial and opportunistic infections ultimately leading to threat to life. Based on strategies to reverse immunosuppression, recent developments in sepsis therapy are focused on molecules having immune enhancing activities. These efforts are focused on defining and revising the immunocompromised status associated with long-term mortality.