• The Korea Journal of Herbology
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• v.27 no.1
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• pp.59-64
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• 2012

Objective : This study was performed to evaluate the effect of Forsythiae Fructus (FF) ethanol extract on inflammatory cytokine production and its underlying mechanisms in mouse macrophages. Methods : Peritoneal macrophages from thioglycollate medium-injected mice were cultured and stimulated with lipopolysaccharide(LPS) or LPS/interferon(IFN)-${\gamma}$ for cytokine measurement and cellular signaling molecule analysis. Results : FF ethanol extract decreased the levels of secreted tumor necrosis factor(TNF)-${\alpha}$ and interleukin(IL)-6 in IFN-${\gamma}$/LPS-stimulated cells in a concentration-dependent manner. FF extract reduced IFN-${\gamma}$/LPS-induced STAT1 phosphorylation and LPS-induced p38 and JNK activation, but not ERK1/2 activity. The extract also inhibited LPS-induced $I{\kappa}B{\alpha}$ degradation through suppression of $I{\kappa}B{\alpha}$ kinase. Conclusions : These results suggest that FF ethanol extract affects the production of TNF-${\alpha}$ and IL-6 through inhibition of activation of STAT-1, $I{\kappa}B{\alpha}$, p38, and JNK.

• Korean Journal of Pharmacognosy
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• v.33 no.3 s.130
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• pp.252-256
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• 2002

In the previous study, we demonstrated that ginsenoside $Rb_1$ isolated from the butanol fraction of the head of Panax ginseng had significant gastroprotective activity on gastritis and gastric ulcer models in rats. It has been well established that drugs to have capacity of scavenging or inhibiting the generation of reactive oxygen radicals prevent the gastric mucosal injury. Ginsenoside $Rb_1$ was tested on HCl ethanol-induced gastritis in rats, DPPH-induced free radical scavenging effect, MDA assay, GSH activity, and SOD activity in gastric tissue. It showed significant inhibition in HCl ethanol-induced gastritis, and al~o significantly increase of GSH activated SOD. We speculate that the protective effect of ginsenoside $Rb_1$ against HCl ethanol-induced gastric mucosal damage is originated from the increase of GSH and the activation of SOD.

• Korean Journal of Veterinary Service
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• v.26 no.4
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• pp.345-359
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• 2003

A number of toxicants have been incriminated as a causing hepatic disease. Among many detrimental injury, alcohol has been noted for hepatitis, fatty liver, fibrosis, and hepatic cirrhosis. The purpose of this study was to develop animal model for hepatic fibrosis in pigs fed ethanol, and to search for a new anti-fibrogenic agent via this model. Twelve male Landrace pigs were divided into 3 groups of 4 animals each. Group 1, 2 and 3 were fed with active ceramic water only, ceramic water + liquid diet containing 15% ethanol and normal tap water + liquid diet containing 15% ethanol for 12 weeks, respectively. At week 12, all pigs were immediately sacrificed for collection each tissue and blood. Serologically, serum ALT and AST levels were significantly reversed in group 2, as compared to group 3. They were normal range in pigs of group 1. Microscopically, macrovesicular lipid droplets and moderate hepatocellular necrosis were evident in the tap water + ethanol fed group 3. However, the active ceramic water treated group 1 showed normal architecture. Moreover, in group 2, mild fatty changes and necrosis were observed in hepatocytes. Collagen fibers were increased in spaces surrounding periportal and interlobular connective tissues in the group 3 of tap water + ethanol, but collagen synthesis and its thickness of fibrotic septa connecting portal tracts were markedly reduced in the group 2 of ceramic water + ethanol. Myofibroblasts were detected mainly in the interlobular connective tissues of pig liver of group 3 treated ethanol and tap water. Few to no myofibroblasts were observed in groups 1 and 2. CYP2E1 was not or rarely detected in group 1 fed ceramic water. However, group 2 showed slightly activation of CYP2E1 in the area of pericentral vein, while CYP2E1 was significantly activated in group 3 fed tap water and ethanol. Based on the above data, we believe that we have developed a unique alcohol induced fibrosis model in pig, which will be useful in developing anti-fibrotic agents and drugs. Furthermore, the active ceramic water used in our study had an inhibitory and may be protective against ethanol induced hepatic toxicity and fibrosis.

• Archives of Pharmacal Research
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• v.19 no.5
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• pp.374-380
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• 1996

Sprague-Dawley male rats (150 g) were chronically treated with 5 v/v % ethanol admixed with nutritionally complete liquid diet and fed ad libitum for 3 weeks. One half of each group was exposed to cold stress at 4 ^{\circ}C either for 24 h (for determination of mRNA by in situ hybridization) or for 48 h (for determination of enzyme activity). Chronic ethanol treatment (ethanol) did not affect tyrosine hydroxylase(TH) mRNA level in locus coeruleus(LC) of brain and adrenal medulla(AM) compared to controls. Cold stress showed strong increase of TH mRNA level in LC and AM compared to controls. Pretreated ethanol reduced the increased TH mRNA level by cold stress in LC and AM. Ethanol did not affect TH activity in LC and adenal glands(adrenals). Cold stress increased TH activity in LC but not in adrenals. Pretreated ethanol did not reduce the increased TH activity by cold stress in LC but this result was not shown in adrenals. Phenylethanolamine-N-methyltransferase(PNMT) activity in $C_{1}$$C_{2}$ and adrenals increased only in ethanol treated group. THese results suggest that ethanol does not affect TH mRNA level and activity in LC and adrenals, but increases PNMT activity in $C_{1}$$C_{2}$ and adrenals in normal rat. It is also suggested that pretreated ethanol reduces the magnitude of cold stress response, that is induction of TH mRNA in LC and AM, and does not reduce the protein activation of TH that is also cold stress response in LC.

• Food Science and Biotechnology
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• v.18 no.2
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• pp.552-555
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• 2009

This study investigated the proapoptotic effect of ethanol extracts obtained from dandelion (Taraxacum officinale) flower on human ovarian cancer SK-OV-3 cells. Cells were treated with dandelion flowers ethanol extract (DFE) ranging from 1.5625 to $100{\mu}g/mL$ for 24 hr. Significant antiproliferative effects of DFE were first observed from at $6.25{\mu}g/mL$ (p<0.05), and this inhibition showed in a dose-dependent manner. When cells were treated with more than $6.25{\mu}g/mL$ DFE, cell-cycle analysis showed that DFE caused an increase in the percentage of sub-G0/G1 cells and arrested at the S and G2/M phase in a dose-dependent manner. Moreover, apoptosis induction by DFE involved p53 activation and bax upregulation as well as downregulation of bcl-2. Our findings indicate that DFE resulted in apoptotic cell death, suggesting that DFE possesses potential anticancer properties.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.139.2-139.2
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• 2003

The in vitro effects of extracted fractions of C. militaris on the secretion of cytokines in murine macrophage cell line, RAW 264.7 were studied. F1 (crude cordycepin containing adenosine), F2 (ethanol precipitation), F3 (ethanol soluble supernatant) and F4 (fraction of through SK-1B) significantly stimulated the production of cytokine and nitric oxide (NO) on murine macrophage cell line RAW264.7. We examined how the ethanol extract of C. militaris regulates production of interleukine 1-beta(IL-1$\beta$), tumor necrosis factor-alpha (TNF-$\alpha$), and NO in vitro. (omitted)

• Journal of Animal Science and Technology
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• v.48 no.3
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• pp.353-360
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• 2006

This study was performed to investigate the effects of artificial stimulation on the increase of the oocyte activation, to evaluate the expression of cyclin B1 protein levels in enucleated mouse oocytes, and to investigate correlation between the oocyte activation and the cyclin B1 protein levels. The oocyte activation was induced by 7% ethanol (EtOH) or 10μg/ml Ca-ionophore with or without 10μg/ml cycloheximide (CH). The activation rate was significantly higher in both single (p<0.05) and combined (p<0.01) stimulated groups compared to control group. The cyclin B1 protein level was significantly reduced in both stimulated groups (p<0.05), except for EtOH+CH treatment group. The expression of cyclin B1 protein showed a higher negative correlation with activation rate in EtOH+CH (r=0.61, p<0.05) and Ca+CH (r=0.86, p<0.01) stimulation groups, but not in a both single stimulation groups. Taken together, it can be suggested that single (EtOH and Ca- ionophore) and combined (EtOH+CH and Ca+CH) stimulation increases the oocyte activation, especially combined stimulation, because it induces the degradation of cyclin B1 protein after artificial stimulation treatments in mouse oocytes.

• YAKHAK HOEJI
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• v.34 no.4
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• pp.267-276
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• 1990

To achieve a better understanding of antioxidant action manifested by malotilate, the dithiol malonates, we monitored the oxy radical-scavenging system against the chronic hepatic damage induced by $CCl_4$ alone or in combination with ethanol. Malotilate was given orally at a dose of 100 mg/kg/day and $CCl_4$ 1.5 ml/kg was injected subcutaneously twice a week for 4 weeks. In each group receiving ethanol, drinking water was replaced by 20% aqueous solution or glucose, isocaloric amounts of ethanol, as a control of ethanol was diluted in its drinking water. Each rat was killed as a starved state at 18 hours after the period of the experiment, four weeks. The results were summarized as follows: 1) Malotilate inhibited the rate of generation of superoxide radicals, the accumulation of lipoperoxides, and promoted the synthesis of glutathione in the liver. 2) Malotilate stimulated the enhancement of activity of superoxide dismutase in hepatic mitochondria. 3) Malotilate had no effects on the hepatic $H_2O_2$ contents. 4) Malotilate showed the increase of catalase activity in the liver poisoned with $CCl_4$, and also gave a tendency to increase it in the liver intoxicated with ethanol. Thus, our data suggested that the activation of hepatic antioxidant system in the presence of malotilate would play a role in protecting liver against the toxic effects of oxy radical and/or lipid peroxides under the hepatotoxic conditions induced by $CCl_4$ with or without ethanol. However, the effects of malotilate against the ethanol-induced hepatotoxicity appear to be insignificant.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2002.11a
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• pp.146-146
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• 2002

Hepatic disease has been noted and reported for involvement various detrimental factors. Among many detrimental injury factors, alcohol has been noted for hepatitis, fatty liver, fibrosis, and hepatic cirrhosis. The purpose of this study is to develop animal model for hepatic fibrosis in pig with ethanol, and to search new anti-fibrogenic agent. Twelve male Landrace pigs were divided into 3 groups of 4 animals each. Group 1, 2 and 3 were fed with ceramic water only, ceramic water + liquid diet containing 20％ ethanol and normal tap water + containing 20％ ethanol for 12 weeks, respectively. At week 12, all pigs were immediately sacrificed for collection each tissue and blood. Serologically, serum ALT and AST levels were significantly reversed in group 2, comparing to group 3. They were normal range in pigs of group 1. Microscopically, macrovesicular lipid droplets and moderate necrosis were evident in the tap water + ethanol fed group 3. However, ceramic water intake group 1 showed normal. Moreover, in group 3, little fatty changes and mild necrosis were observed. Collagen fibers were detected in the spaces of surrounding periportal and interlobular areas in the group 3 of tap water + ethanol, but collagen synthesis and its thickness of fibrotic septa connecting portal tracts was markedly reduced in the group 2 of ceramic water + ethanol. In immunohistochemistry, myofibroblasts were detected in the ethanol and tap water treated group 3. No or a few myofibroblasts were observed in groups 1 and 2. CYP 2E1 was rarely detected in group 1 fed ceramic water. However, group 2 showed slightly activation of CYP 2E1 in the area of pericentral, while CYP 2E1 was significantly activated in group 3 fed tap and ethanol. Taken together above, alcohol fibrosis model in pig was established. Furthermore, ceramic water had an inhibitory and protecting ability for alcohol-induced hepatic damages.

• Bulletin of the Korean Chemical Society
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• v.24 no.9
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• pp.1293-1302
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• 2003

Rate constants at various temperatures and activation parameters are reported for solvolyses of acyl chlorides (RCOCl), with R = Me, Et, i-Pr, t-Bu, cyclopentylmethyl, benzyl, thiophenylmethyl, 2-phenylethyl, diphenylmethyl, and phenylthiomethyl in 100% ethanol, 100% 2,2,2-trifluoroethanol (TFE), 80% v/v ethanol/ water and 97% w/w TFE/water. Additional rate constants for solvolyses with R = Me, t-Bu, and $PhCH_2$ are reported for TFE/water and TFE/ethanol mixtures, and for solvolyses with R = t-Bu, and PhCH2 are reported for 1,1,1,3,3,3-hexafluoropropan-2-ol/water mixtures, as well as selected kinetic solvent isotope effects (MeOH/MeOD and TFE). Taft plots show that electron withdrawing groups (EWG) decrease reactivity significantly in TFE, but increase reactivity slightly in ethanol. Correlation of solvent effects using the extended Grunwald-Winstein (GW) equation shows an increasing sensitivity to solvent nucleophilicity for EWG. The effect of solvent stoichiometry in assumed third order reactions is evaluated for TFE/ethanol mixtures, which do not fit well in GW plots for R = Me, and t-Bu, and it is proposed that one molecule of TFE may have a specific role as electrophile; in contrast, reactions of substrates containing an EWG can be explained by third order reactions in which one molecule of solvent (ethanol or TFE) acts as a nucleophile, and a molecule of ethanol acts as a general base catalyst. Isokinetic relationships are also investigated.