• Food Engineering Progress
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• v.23 no.2
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• pp.118-124
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• 2019

This study aims to investigate the physical properties of extruded psyllium husk upon the addition of emulsifiers. Three different emulsifiers-glycerol monostearate (GMS), polyglycerol ester (PGE), and sugar ester (SE)-were added to the mixture of psyllium husk and rice powder before extrusion. Extrusion was performed using a twin-screw extruder at 140℃ die temperature, 200 rpm screw speed, and 16% feed moisture content. The physical properties of psyllium husk extrudates including expansion ratio, specific length, piece density, texture profile, color properties, water soluble index, and water absorption index were evaluated. It was observed that the expansion ratio was the highest while the specific length and piece density were the lowest in the control which had no emulsifiers. Texture profile analysis showed that the apparent elastic modulus and breaking strength were highest in the extrudate with a PGE of 0.1%. The adhesiveness was found to be lowest in the extrudates with an SE of 0.1% and GMS of 0.5%. Lightness value was highest in the extrudate with a PGE of 0.1%. Color difference, water soluble index, and water absorption index were highest in the control. The results reveal that some physical properties of extruded psyllium husk were improved with the addition of emulsifiers. This finding provides useful information for the development of psyllium snacks with good physical characteristics.

• Archives of Pharmacal Research
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• v.28 no.9
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• pp.1013-1018
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• 2005

A number of 1,5-diarylimidazoles has been synthesized and evaluated for their inhibitory activities of COX-2 catalyzed $PGE_2$ production. 1,5-Diarylimidazoles were obtained from imimes and p-toluenesulfonylmethyl cyanide (TosMIC). Imines were prepared from commercially available amines and aldehydes. Among the compounds tested, 1-(2,4-difluorophenyl)-5-(4­methylsulfonylphenyl)imidazole (2r) showed strong inhibitory activity, however, most diarylimidazoles exhibited little to low inhibitory activities against COX-2 catalyzed $PGE_2$ production.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.193.2-193.2
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• 2003

Phytochemical examination of Sophorae Fructus yielded six phenolic compounds. The structures were elucidated as genistein(1), genistin(2) and genistein 7-O-${\alpha}$- L-rhamnopyranoside(3) by phytochemical and spectral evidences. The other compounds(4, 5, 6) are understudied by 2D-NMR. Nitric Oxide and PGE$_2$ production inhibitory activities in INF-${\gamma}$, LPS stimulated RAW 264.7 cell were examined. Compound 2 and 4 showed significant nitrogen monoxide(NO) production inhibitory activity in IFN-${\gamma}$, LPS stimulated RAW 264.7 cell. (omitted)

• The Journal of Internal Korean Medicine
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• v.30 no.1
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• pp.36-50
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• 2009

Objectives : This study was aimed to verify the cytoprotective function, antioxidative effect and inflammation genes inhibitory effects of Lycium chinense Milie. Therefore the generation of superoxide anion radical ( $O_2\;^-$), peroxynitrite ($ONOO^-$), nitric oxide (NO) and prostaglandin $E_2$ $(PGE_2)$ was investigated in the renal epithelial cells of mouse. Effects of Lycium chinense Milie on the expression of inflammation-related proteins, $IKK-{\alpha}$. $p-IKK-\alpha\beta$, $p-I{\kappa}B-\alpha$, $NF-{\kappa}B$ (p50, p65), COX-2 and iNOS, were examined by western blotting. Methods : For this study, the fluorescent probes were used, namely dihydrorhodamine 123 (DHR 123), 4.5-diaminofluorescein (DAF-2) and 2',7'-dichlorodihydrofluorescein diacetate (DCFDA). Western blotting was performed using anti-$IKK-\alpha$, anti-phospho $IKK-\alpha\beta$, anti-phospho $I{\kappa}B-\alpha$, anti-$NF-{\kappa}B$ (p50, p65), anti-COX-2 and anti-iNOS, respectively. Results : Lyciutn chinense Milie reduced $H_{2}O_{2}$-induced cell death dose-dependently. It inhibited the generation of $O_2\;^-$, $ONOO^-$, NO and $PGE_2$ in the $H_{2}O_{2}$-treated renal epithelial cells of mouse in vitro. Lycium chinense Milie inhibited the expression of $IKK-\alpha$, $p-IKK-\alpha\beta,\;p-I{\kappa}B-\alpha$, COX-2 and iNOS genes by means of decreasing activation of $NF-{\kappa}B$. Conclusions : According to above results. Lycium chinense Milie recommended to be applied in treatment for the inflammatory process and inflammation-related diseases.

• YAKHAK HOEJI
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• v.52 no.1
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• pp.85-91
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• 2008

8-Acyl and 8-sulfonylamidowogonin analogues were synthesized as potential anti-inflammatory agents. Nitration of 5,7-dihydroxyflavone (chrysin) followed by methylation of phenol groups and reduction of nitro group yielded 8-aminowogonin analogues. Acylation and sufonylation of 8-aminowogonin followed by demethylation reactions gave the title compunds. The synthesized wogonin analogues showed much reduced inhibitory activity on prostaglandin $E_2\;(PGE_2)$ production.

• Bulletin of the Korean Chemical Society
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• v.33 no.1
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• pp.305-308
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• 2012

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.5
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• pp.507-512
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• 1999

Contribution of prostaglandins $D_2,\;E_2\;and\;I_2\;(PGD_2,\;PGE_2\;and\;PGI_2)$ on the regulation of ATP-sensitive $K^+$ channel $(K_{ATP}\;channel)$ was investigated in isolated single rat ventricular cardiac myocytes using the patch clamp technique. $PGD_2,\;PGE_2\;and\; PGI_2$ did not affect $K_{ATP}$ channel activity in the inside-out patch, but increased channel activity in a dose-dependent manner when the channel activities were attenuated by the administration of 100 ${\mu}M$ ATP to the internal solution in the inside-out patch. Channel activations by the prostaglandins were abolished by 50 ${\mu}M$ glibenclamide, a $K_{ATP}$ channel blocker. Dose-response curves of relative channel activity against the ATP concentrations of internal solution in the inside-out patch were shifted to the right in the presence of those three prostaglandins. The rank order of the channel stimulatory potencies $(as\;IC_{50}\;for\;ATP)$ calculated from the dose-response curves were $PGI_2\;>\;PGD_2\;>\;PGE_2.$ Conductance of the channel was not changed by those three prostaglandins. In conclusion, we suggest that prostaglandins $D_2,\;E_2\;and\;I_2$ are involved in the regulation of $K_{ATP}$ channel activity in certain circumstances, and that those three prostaglandins may cause myocardial relaxation by opening $K_{ATP}$ channels, thus protecting the heart from ischema.

• Journal of Nutrition and Health
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• v.37 no.3
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• pp.182-192
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• 2004

Conjugated linoleic acid (CLA) is the mixture of positional and geometric isomers of linoleic acid (LA), which is found abundantly in dairy products and meats. This study was performed to investigate the anticarcinogenic effect of CLA in HepG2 hepatoma cells. HepG2 cell were treated with LA and CLA at the various concentrations of 10, 20, 40, 80 uM each at different incubation times. After each incubation times, cell proliferation, fatty acids incorporation into cell, peroxidation and postaglandin E$_2$ (PGE$_2$) and thromboxane $A_2$ (TXA$_2$) for the eicosanoid metabolism were measured. LA treated HepG2 cells were increased cell growth 6 - 70％ of control whereas CLA increased cell death the half of those in LA group (p 〈 0.001). LA and CLA were incorporated very well into the cellular membranes four times higher than in control according to concentration and longer incubation times. Moreover, LA synthesized significantly arachidonic acids corresponding with LA concentration compared to CLA supplementation. The supplementation with LA increased intracellular lipid peroxides concentration corresponding with LA concentration and five times higher than those in CLA significantly at any incubation times (p 〈 0.001). PGE$_2$ and TXA$_2$ levels were three to twenty times lower in condition of CLA treatments than LA, respectively. Overall, the dietary CLA might change the HepG2 cell growth by the changes of cell composition, production of lipid peroxide. Since CLA have not changed the levels of arachidonic acid of cell membrane, which was sources of eicosanoids, eicosanoid synthesis was not increased in CLA compared to LA. Our results was suggest CLA has a possibility to protect the progress of atherosclerosis because CLA does not produce lipid production and endothelial contraction factors in liver.

• Parasites, Hosts and Diseases
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• v.44 no.3
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• pp.197-207
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• 2006

This experiment focused on MAPK activation in host cell invasion and replication of T. gondii, as well as the expression of CC chemokines, MCP-1 and $MIP-1\alpha$, and enzyme, COX-2/prostaglandin $E_2(PGE_2)$ in infected cells via western blot, $[^3H]-uracil$ incorporation assay, ELISA and RT-PCR. The phosphorylation of ERK1/2 and p38 in infected HeLa cells was detected at 1 hr and/or 6 hr postinfection (PI). Tachyzoite proliferation was reduced by p38 or JNK MAPK inhibitors. MCP-1 secretion was enhanced in infected peritoneal macrophages at 6 hr PI. $MIP-1\alpha$ mRNA was increased in macrophages at 18 hr PI. MCP-1 and $MIP-1\alpha$ were reduced after treatment with inhibitors of ERK1/2 and JNK MAPKs. COX-2 mRNA gradually increased in infected RAW 264.7 cells and the secretion of COX-2 peaked at 6 hr PI. The inhibitor of JNK suppressed COX-2 expression. $PGE_2$ from infected RAW 264.7 cells was increased and synthesis was suppressed by PD98059, SB203580, and SP600125. In this study, the activation of p38, JNK and/or ERK1/2 MAPKs occurred during the invasion and proliferation of T. gondii tachyzoites in HeLa cells. Also, increased secretion and expression of MCP-1, $MIP-1\alpha$, COX-2 and $PGE_2$ were detected in infected macrophages, and appeared to occur via MAPK signaling pathways.

• Environmental Analysis Health and Toxicology
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• v.22 no.2 s.57
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• pp.137-145
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• 2007

The effect of cadmium chloride $(CdCl_2)$ on the expression of E-cadherin was examined in bEnd.3 mouse brain endothelial cells. $CdCl_2$ induced $PGE_2$ release, which were blocked by non-steroidal antinflamatory drugs (NSAIDs) such as indomethacin and NS398 indicating the expression of COX-2 might contribute to $PGE_2$ production. $CdCl_2$ decreased the expression of E-cadherin, but not VE-cadherin at levels of mRNA and protein. Reduced expression level of E-cadherin was restored by NSAIDs, which was reversed by the addition of $PGE_2$. $CdC_2$-induced decrease of E-cadherin level was also recovered by antioxidants including N-acetylcyteine (NAC) and trolox. Together with previous report which showed $CdCl_2$ induced COX-2 expression in a cellular oxidative stress dependent manner, these data suggest that $CdCl_2$ decreases E-cadherin expression through induction of cellular oxidative stress and in turn COX-2 expression in brain endothelial cells.