• The Journal of Korean Obstetrics and Gynecology
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• v.15 no.4
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• pp.61-75
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• 2002

Recombinant human $interleukin-1{\beta}$ $(rhIL-1{\beta})$ regulates several activities of the osteoblast cells derived from mouse calvarial bone explants in vitro. $rhIL-1{\beta}$ stimulated cellular proliferation and the synthesis of prostaglandin $E_2(PGE_2)$ and plasminogen activator activity in the cultured cells in a dose-dependent manner. However, the induction of osteocalcin synthesis and alkaine phosphatase activity in response to vitamine D, two characteristics of the osteoblast phenotype, were antagonized by $rhIL-1{\beta}$ over a similar dose range. This study supports the role of $IL-1{\beta}$ in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by $IL-1{\beta}$. When the mouse calvarial bone cells were used, the bone resorption induced by $IL-1{\beta}$ was strongly inhibited by calcitonin treatment, indicating osteoclast-mediated bone resorption. On the other hand, the medicinal extracts of Taeyoungjon-Jahage (T.Y.J-J.H.G extracts) was tested for whether they could inhibit $IL-1{\beta}-induced$ $PGE_2$ production. Cell viability was not significantly affected by treatment with the indicated concentration of the extracts. The T.Y.J.-J.H.G. extracts were shown to have the inhibitory effects against the synthesis of $PGE_2$. We also examined the effect of the pretreatment with a various concentrations of the T.Y.J.-J.H.G. extracts then treated the $PGE_2-induction$ agents. Pretreatment of the T.Y.J.-J.H.G. extracts for 1 h, which by itself had little effect on cell survival, did not enhance the synthesis of $PGE_2$. Furthermore, the T.Y.J-J.H.G. extracts were shown to have the protective effects against plasminogen dependent fibrinolysis induced by the bone resorption agents of $IL-1{\beta}$. Pretreatment of the T.Y.J.-J.H.G. extracts for 1 h did not enhance the plasminogen dependent fibrinolysis. Finally, calcitonin showed the inhibitory activity the $IL-1{\beta}-stimulated$ bone resorption in the mouse calvarial bone cells having both of the osteoblast and osteoclast cells. Seemingly, pretreatment of the T.Y.J.-J.H.G. extracts for 1 h reduced the bone resorption. These results clearly indicated that calcitonin and T.Y.J.-J.H.G. extracts play key roles in inhibition of the osteoclast-mediated bone resorption.

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.1
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• pp.13-24
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• 2006

Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride $(CoCl_2)$ has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by $CoCL_2$ and effects of EGCG on $CoCl_2-induced$ apoptosis in PC12 cells. Administration of $CoCl_2$ decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with $100{\mu}M$ EGCG for 30 min before PC12 cells were exposed to $150{\mu}M$ $CoCl_2$, being resulted in the cell viability and DNA fragmentation being rescued. $CoCl_2$ caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by $CoCl_2$. EGCG suppressed the apoptotic peak and a loss of ${\Delta}{\psi}_m$ induced by $CoCl_2$. $CoCl_2$ decreased Bcl-2 expression but Bax expression was not changed in $CoCl_2$- treated cells. EGCG attenuated the Bcl-2 underexpression by $CoCl_2$. $CoCl_2$ augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ apoptosis in PC12 cells.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.703-712
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• 1995

Background: Peripheral blood monocytes are important immune effector cells that play a fundamental role in cellular immunity. In addition to their antigen-presenting and phagocytic activities, monocytes/macrophage produce a vast array of regulatory and chemotactic cytokines. Interleukin-8(IL-8), a potent neutrophil-activating and chemotactic peptide, is produced in large quantities by mononuclear phagocytes and may be an important mediator of local and systemic inflammation. Overexpression by IL-8 of such inflammation may be an important step of tissue injury frequently seen in inflammatory reaction. So it could be hypothesized that the agents which block the production of IL-8 can decrease the inflammatory reaction and tissue injury. To evaluate this, we described the effect of Dexamethasone, $PGE_2$, Indomethacin and Interferon-$\gamma$(IFN-$\gamma$) on IL-8 mRNA and protein expression from LPS-stimulated human peripheral blood monocytes(PBMC). Method: PBMC was isolated from healthy volunteers. To evaluate the effect of Dexamethasone, $PGE_2$ & Indomethacin, these drug were treated for 1 hour before and after LPS stimulation and IFN-$\gamma$ was only treated I hour before the LPS stimulation. Northern blot analysis for IL-8 mRNA and ELISA for immunoreactive IL-8 protein in culture supernatant were performed. We repeated above experiment three times for Northern blot analysis and two times for ELISA and got the same result. Results: 1) Pre- and post-treatment of Dexamethasone suppressed both the LPS stimulated IL-8 mRNA expression and IL-8 protein release in PBMC. 2) IFN-$\gamma$ pre-treatment suppressed the IL-8 mRNA expression and IL-8 protein release in unstimulated cells. 3) In LPS stimulated cells, IFN-$\gamma$ suppressed the IL-8 mRNA expression but IL-8 protein release suppression was not observed. 4) $PGE_2$ and Indomethacin exert no effect on the LPS-stimulated IL-8 mRNA and protein expression in concentration used in this experiment ($PGE_2;10^{-6}M$, Indomethacin; $10{\mu}M$). Conclusion: One of the mechanism of antiinflammatory action of Dexamethasone can be explained by the suppressing effect of IL-8 production in some extent and by this antiinflammatory effect, dexamethasone can be used to suppress local and systemic inflammation mediated by IL-8.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.36 no.2
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• pp.157-165
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• 2010

In this study, the antioxidative effects, inhibitory effects on tyrosinase and elastase of Rhododendron brachycarpum D. Don extracts were investigated. And the moisturizing effect of cream containing R. brachycarpum D. Don extract were investigated by clinical trial. The ethyl acetate fraction of R. brachycarpum D. Don extract (1.83 ${\mu}g/mL$) showed the most prominent the free radical (1,1-diphenyl-2-picrylhydrazyl, DPPH) scavenging activity ($FSC_{50}$). Reactive oxygen species (ROS) scavenging activities ($OSC_{50}$) of R. brachycarpum D. Don extracts on ROS generated in $Fe^{3+}$-EDTA/$H_2O_2$ system were investigated using the luminol-dependent chemiluminescence assay. The 50 % extract fraction (0.064 ${\mu}g/mL$) showed the most prominent ROS scavenging activity. The protective effects of extract/fractions of R. brachycarpum D. Don on the rose-bengal sensitized photohemolysis of human erythrocytes were investigated. The R. brachycarpum D. Don extracts suppressed photohemolysis in a concentration dependent manner (1 ~ 10 ${\mu}g/mL$). The inhibitory effects ($IC_{50}$) of R. brachycarpum D. Don extracts on tyrosinase were determined with ethyl acetate fraction of R. brachycarpum D. Don extract (70.5 ${\mu}g/mL$) and aglycone fraction of extract (122.40 ${\mu}g/mL$). The inhibitory effects ($IC_{50}$) on elastase were determined with ethyl acetate of R. brachycarpum D. Don extract (43.50 ${\mu}g/mL$) and aglycone fraction of extract (20.73 ${\mu}g/mL$). The cream containing the ethyl acetate fraction of R. brachycarpum D. Don extracts was formulated for skin hydration effect and transepidermal water loss (TEWL). The cream containing R. brachycarpum D. Don extract was applied to the right lower arm. After 180 min, the water contents in skin were increased by 1 ~ 4 % than the placebo cream. And TEWL of parts was decreased as 7.7 $g/m^2h$ (experimental cream) and 8.9 $g/m^2h$ (placebo cream) respectively. These results indicate that extract/fractions of R. brachycarpum D. Don can function as antioxidants in biological systems, particularly skin exposed to UV radiation by scavenging $^1O_2$ and other ROS, and protect cellular membranes against ROS. And inhibitory activity on tyrosinase of the aglycone fraction could be applicable to new functional cosmetics for whitening and anti-wrinkle products. Also the increase of skin hydration of the cream containing extract could be applicable to new functional cosmetics for antiaging.

• Food Science and Preservation
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• v.22 no.1
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• pp.27-35
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• 2015

Anti-obese effects of mulberry (Morus alba L.) root bark was investigated in vitro by measuring its inhibitory effect against 3T3-L1 preadipocyte differentiation and digestive enzymes such as ${\alpha}$-amylase, ${\alpha}$-glucosidase and pancreatic lipase. Ethanol extract of mulberry root bark (MRE) showed the potent inhibitory activities on ${\alpha}$-amylase, ${\alpha}$-glucosidase and pancreatic lipase with $IC_{50}$ values of $7.86{\pm}0.36$, $0.12{\pm}0.03$ and $7.93{\pm}0.11mg/mL$, respectively. Furthermore, MRE significantly suppressed cellular lipid accumulation in 3T3-L1 cells in a dose-dependent manner. To elucidate the mechanism of MRE, we performed qRT-PCR and Western blotting for the expression of genes related with adipogenesis and lipogenesis. Treatment of MRE markedly suppressed the protein expression of $PPAR{\gamma}$, $C/EBP{\alpha}$ and SREBP-1c, as well as FAS and ACC, which are the key transcription factors and metabolic enzymes in adipogenesis and lipogenesis. In addition, qRT-PCR analysis indicated that the anti-adipogenesis effect of MRE might be due to its inhibition at transcription levels. These results demonstrate that MRE can effectively suppress adipocyte differentiation and inhibit key enzymes related to obesity. Our findings suggest that mulberry root bark may have a potential benefit in preventing obesity.

• KSBB Journal
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• v.18 no.1
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• pp.55-61
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• 2003

To isolate and purify the antimicrobial and antitumor agents in Xanthium strumarium L. hydrothermal extract. The crude extract was extracted in ether or ethylacetate under neutral, acidic, and alkali conditions. The antimicrobial activity of each extract was tested against 16 strains of bacteria, 2 strains of yeast, and 2 strains of fungus. The ether neutral extract (XE-N) exhibited the strongest growth inhibition upon the 8 strains of gram-positive bacteria, 6 strains of gram-negative bacteria and Cryptococcus neoformans. Fluorescein diacetate (FDA) testing of XE-N and XEA-N showed growth inhibition of the 3 strains of E. coli, S. aureus and C. albicans even at 30 ng/mL, with the exception of p. aeruginosa. XE-N-S1 and XE-N-S3 from neutral ether extract (XE-N), XE-N-S3 from the acidic ether extract (XE-A), and XEA-N-S1 from ethylacetate (XEA-N) were purified as antimicrobial and antitumor agents. However all purified compounds decomposed with the exception of XE-N-S1. The results upon the antitumor activities of the crude extract and of its purified compounds, showed that XE-N-S1 had the best antitumor activity against HeLa cells. In terms of antitumor activity against HepG2 cells, XE-N-S1 and XE-N-S3 were superior, and against HT29 cells XE-N and XE-N-Sl were good, against Saos2, NCI H522, NCI H1703, Clone M3 cells XE-N-51 was very good, and against LN CAP cells XE-N-S3 was the best. Comparing of cellular toxicities various extracts and purified compounds with the existing antitumor agents, XE-A, XEA-A and XEA-B had the lowest toxicity, and XE-B had a lower toxicity than etoposide. XE-N-S1 and XE-N-S3 showed higher toxicities than etoposide, and the toxicity of XE-A-S3 was higher than that of etoposide, and lower than that of csplatin.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.163-170
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• 2006

Nardostachyos Rhizoma (N. Rhizoma) belonging to the family Valerianaceae has been anti-arrhythmic effect, and sedation to the central nerve and a smooth muscle. We reported that the water extract of N. Rhizoma induced apoptotic cell death and differentiation in human promyelocytic leukemia (HL-60) cells. Cytotoxicity of N. Rhizoma was detected only in HL-60 cells (IC50 is about 200 ${\mu}g/ml$). The cytotoxic activity of N. Rhizoma in HL-60 cells was increased in a dose-dependent manner. We used several measures of apoptosis to determine whether these processes were involved in N. Rhizoma-induced apoptotic cell death. The high-dose (200 ${\mu}g/ml$) treatment of N. Rhizoma to HL-60 cells showed cell shrinkage, cell membrane blobbing, apoptotic bodies, and the fragmentation of DNA, suggesting that these cells underwent apoptosis. Treatment of HL-60 cells with N. Rhizoma time-dependently induced activation of caspase-3, caspase-8, and caspase-9 and proteolytic cleavage of poly(ADP-ribose) polymerase. Also, we investigated the effect of N. Rhizoma on cellular differentiation and proliferation in HL-60 cells. Differentiation and proliferation of HL-60 cells was determined through expression of CD11b and CD14 surface antigens using flow cytometry and nitroblue tetrazolium (NBT) assay, and through analysis of cell cycle using propidium iodide assay, respectively. N. Rhizoma induced the differentiation of HL-60 at the low-dose (100 ${\mu}g/ml$) treatment, as shown by increased expression of differentiation surface antigen CD11b, but not CDl4 and increased reducing activity of NBT. When HL-60 cells were treated with N. Rhizoma at concentration of $50{\mu}g/ml\;and\;100{\mu}g/ml$, NBT-reducing activities induced approximately 1.5-fold and 20.0-fold as compared with the control. In contrast, HL-60 cells treated with the N. Rhizoma-ATRA combination showed markedly elevated levels of 26.3-fold at $50{\mu}g/ml$ N. Rhizoma-0.1 ${\mu}M$ ATRA combination and 27.5-fold at 50 ${\mu}g/ml$ N. Rhizoma-0.2 ${\mu}M$ ATRA combination than when treated with N. Rhizoma alone or ATRA alone. It may be that N. Rhizoma plays important roles in synergy with ATRA during differentiation of HL-60 cells. DNA flow-cytometry indicated that N. Rhizoma markedly induced a G1 phase arrest of HL-60 cells. N. Rhizoma-treated HL-60 cells increased the cell population in G1 phase from 32.71% to 42.26%, whereas cell population in G2/M and S phases decreased from 23.61% to 10.33% and from 37.78% to 33.98%, respectively. We examined the change in the $p21^{WAF1/Cip1}\;and\;p27^{Kip1}$ proteins, which are the CKIs related with the G1 phase arrest. The expression of the CDK inhibitor $p27^{Kip1},\;but\;not\;p21^{WAF1/Cip1}$ were markedly increased by N. Rhizoma. Taken together, these results demonstrated that N. Rhizoma induces apoptotic cell death through activation of caspase-3, and potently inhibits the proliferation of HL-60 cells via the G1 phase cell cycle arrest in association with $p27^{Kip1}$ and granulocytic differentiation induction .

• Korean Journal of Food Science and Technology
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• v.49 no.4
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• pp.430-437
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• 2017

The protective effect of Pteridium aquilinum on high glucose-induced cytotoxicity was examined in vitro to investigate the relationship between diabetic condition and neuronal dysfunction. The ethyl acetate fraction of P. aquilinum (EFPA), with total phenolic content of 265.08 mg gallic acid equivalent/g, showed higher 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid)/2,2-diphenyl-1-picrylhydrazyl radical scavenging activities and lipid peroxidation inhibitory effect than any other fraction. In addition, EFPA showed a significant reduction in the inhibitory effect on ${\alpha}$-glucosidase activity ($IC_{50}$ value=$205.26{\mu}g/mL$) compared to the acarbose positive control. The anti-oxidative effect in PC12 cells, protective effects on high glucose-induced oxidative stress in neuronal cells, and neurotoxicity were measured using 2',7'-dichlorofluorescin diacetate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide, and lactate dehydrogenase assays, respectively. EFPA showed conspicuous inhibitory effect on cellular reactive oxygen species production and neuronal cell apoptosis. Finally, kaempferol-3-glucoside was identified as the main phenolic compound of EFPA using high performance liquid chromatography.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.34 no.3
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• pp.189-200
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• 2008

In this study, the antioxidative effects, inhibitory effects on elastase, and components of Quercus glauca extracts were investigated. The free radical (1,1-diphenyl-2-picrylhydrazyl, DPPH) scavenging activity $(FSC_{50})$ of extract I fractions of Quercus glauca leaf was in the order: 50% ethanol extract $(12.45{\mu}g/mL)$ < ethyl acetate fraction $(10.47{\mu}g/mL)$ < deglycosylated flavonoid aglycone fraction $(8.57{\mu}g/mL)$. Reactive oxygen species (ROS) scavenging activities $(OSC_{50})$ of some Quercus glauca leaf extracts on ROS generated in $Fe^{3+}-EDTA/H_2O_2$ system were investigated using the luminol-dependent chemiluminescence assay. The order of ROS scavenging activity was 50% ethanol extract $(OSC_{50},\;4.2{\mu}g/mL)$ < deglycosylated flavonoid aglycone fraction $(1.58{\mu}ug/mL)$ < ethyl acetate fraction $(0.66{\mu}g/mL)$. Ethyl acetate fraction showed the most prominent scavenging activity. The protective effects of extract / fractions of Quercus glauca leaf on the rose-bengal sensitized photohemolysis of human erythrocytes were investigated. The Quercus glauca leaf extracts suppressed photohemolysis in a dose dependent manner, particularly deglycosylated flavonoid aglycone fraction exhibited the most prominent celluar protective effect $({\tau}_{50}$, 398.67 min at $50{\mu}g/mL$). Aglycone fractions obtained from the deglycosylation reaction of ethyl acetate fraction among the Quercus glauca leaf extracts, showed 2 bands in TLC and 2 peaks in HPLC experiments (360 nm) as well. Two components were identified as quercetin (55.77%), and kaempferol (44.23 %). TLC chromatogram of ethyl acetate fraction of Quercus glauca leaf extracts revealed 6 bands $(QG1{\sim}QG6)$, Among them, isoquercitrin (QG3), hyperin (QG4), and rutin (QG6) were identified. The inhibitory effect of aglycone fraction on tyrosinase $(IC_{50},\;73.5{\mu}g/mL)$ and elastase $(IC_{50},\;16.2{\mu}g/mL)$ was high. These results indicate that extract / fractions of Quercus glauca can function as antioxidants in biological systems, particularly skin exposed to UV radiation by scavenging $^1O_2$ and other ROS, and protect cellular membranes against ROS. And component analysis of Quercus glauca leaf extract and inhibitory activity on tyeisinase and elastase of the aglycone fraction could be applicable to new functional cosmetics.

• Korean Journal of Food Science and Technology
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• v.53 no.4
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• pp.423-433
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• 2021

This study was performed to examine the neuroprotective effect of the ethyl acetate fraction from Eucommia ulmoides oliver leaf (EFEL) on PM_2.5-induced cytotoxicity. EFEL had higher total phenolic and flavonoid contents than the other fractions. In ABTS and DPPH radical scavenging activities, the IC₅₀ of EFEL was measured as 212.80 and 359.13 ㎍/mL, respectively. To investigate the neuroprotective effect of EFEL, MTT and DCF-DA assays were performed on HT22, MC-IXC, and BV-2 cells. EFEL effectively decreased PM_2.5-induced intercellular reactive oxygen species (ROS) content and inhibited PM_2.5-induced cell death. In the results of protein expression related to cellular cytotoxicity on microglial cells (BV-2), EFEL had an improvement effect on cell apoptosis and inflammatory pathways. Rutin and chlorogenic acid were identified as the main physiological compounds. Moreover, it was expected that EFEL, including rutin and chlorogenic acid, could be functional food substances with neuroprotective effects against PM_2.5-induced oxidative stress.