• Korean Journal of Poultry Science
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• v.38 no.1
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• pp.37-43
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• 2011

The effect of cecal ligation on the utilization of dietary [15N]urea in chickens fed 5 % protein diet plus urea were investigated. Nitrogen balance and utilization tended (P<0.01) to increase by cecal ligation. Total uric acid excretion was significantly decrease by (P<0.01) cecal ligation in chickens from origin of diet and urea (P<0.01). Excretion of ammonia was increased in chickens from origin of diet, where as it decreased in chickens an urea diet (P<0.01). Amount of urea nitrogen excretion from origin of urea was significantly decrease (P<0.01) by cecal ligation, but cecal ligated chicken fed 5% protein diet with urea showed 51.6% urea utilization. Result obtained in present study indicates that ceca is having beneficial role for urea utilization in chicken fed protein deficient diets, but ceca do not always positive role for nitrogen utilization.

• Korean Journal of Poultry Science
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• v.29 no.4
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• pp.259-263
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• 2002

It was examined whether the ceca and the back-flow of urine into the lower intestine are involved in water intake and excretion in chickens and food intake affects those. Colostomy significantly increased water intake, total water excretion and the ratio of the water intake to food intake in the ceca-ligated chickens under restrict and ad libitum feeding conditions (P<0.05), but the increases were much larger in chickens fed ad libitum than in those fed restrictedly. Cecal ligation increased water intake, total water excretion and the ratio of water intake to food intake in the colostomised chickens which were fed freely (P<0.05). but not in those fed restrictedly, None of colostomy and cecal ligation affected the resultant water balances in chickens under both feeding conditions. Colostomy increased food intake in the ceca-ligated chickens (P<0.05), but no increase by cecal ligation was observed in colostomised chickens. It is concluded that the lower intestine takes a very important role in water recovery from urine to maintain water balance in chickens.

• Molecules and Cells
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• v.44 no.12
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• pp.893-899
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• 2021

BLT2 is a low-affinity receptor for leukotriene B₄, a potent lipid mediator of inflammation generated from arachidonic acid via the 5-lipoxygenase pathway. The aim of this study was to investigate whether BLT2 plays any role in sepsis, a systemic inflammatory response syndrome caused by infection. A murine model of cecal ligation and puncture (CLP)-induced sepsis was used to evaluate the role of BLT2 in septic inflammation. In the present study, we observed that the levels of ligands for BLT2 (LTB₄ [leukotriene B₄] and 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid]) were significantly increased in the peritoneal lavage fluid and serum from mice with CLP-induced sepsis. We also observed that the levels of BLT2 as well as 5-lipoxygenase (5-LO) and 12-LO, which are synthesizing enzymes for LTB₄ and 12(S)-HETE, were significantly increased in lung and liver tissues in the CLP mouse model. Blockade of BLT2 markedly suppressed the production of sepsis-associated cytokines (IL-6 [interleukin-6], TNF-α [tumor necrosis factor alpha], and IL-1β [interleukin-β] as well as IL-17 [interleukin-17]) and alleviated lung inflammation in the CLP group. Taken together, our results suggest that BLT2 cascade contributes to lung inflammation in CLP-induced sepsis by mediating the production of inflammatory cytokines. These findings suggest that BLT2 may be a potential therapeutic target for sepsis patients.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.229-229
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• 2002

Although hepatocellular dysfunction occurs during sepsis. the mechanism responsible for this remains unclear. Since Kupffer cells provide signals that regulate hepatic response in endotoxin and inflammation. the aim of this study was to investigate the role of Kupffer cells in the alterations in the hepatic microsomal drug metabolizing function during sepsis. Rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP)followed by fluid resuscitation. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.1
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• pp.1-7
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• 2015

Our previous study has shown berberine prevents damage to the intestinal mucosal barrier during early phase of sepsis in rat through mechanisms independent of the NOD-like receptors signaling pathway. In this study, we explored the regulatory effects of berberine on Toll-like receptors during the intestinal mucosal damaging process in rats. Male Sprague-Dawlay (SD) rats were treated with berberine for 5 d before undergoing cecal ligation and puncture (CLP) to induce polymicrobial sepsis. The expression of Toll-like receptor 2 (TLR 2), TLR 4, TLR 9, the activity of nuclear factor-kappa B ($NF-{\kappa}B$), the levels of selected cytokines and chemokines, percentage of cell death in intestinal epithelial cells, and mucosal permeability were investigated at 0, 2, 6, 12 and 24 h after CLP. Results showed that the tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) level were significantly lower in berberine-treated rats compared to the control animals. Conversely, the expression level of tight junction proteins, percentage of cell death in intestinal epithelial cells and the mucosal permeability were significantly higher in berberine-treated rats. The mRNA expression of TLR 2, TLR 4, and TLR 9 were significantly affected by berberine treatment. Our results indicate that pretreatment with berberine attenuates tissue injury and protects the intestinal mucosal barrier in early phase of sepsis and this may possibly have been mediated through the TLRs pathway.

• Korean Journal of Oriental Medicine
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• v.15 no.3
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• pp.75-82
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• 2009

Anti-mutagenic and anti-septic effects of $\beta$-1,3/1,6-glucan from Aureobasidium pullulans SM-2001 were evaluated on the on the cyclophosphamide (CPA)-cecal ligation puncture (CLP) and CPA-treated mice. To induce immunosuppression and mutagenicity, 150 and 110 mg/kg of CPA were single intraperitoneally injected at 3 or 1 day before CLP or initial $\beta$-glucan administration. In CLP animals, the cecum was mobilized and ligated below the ileocecal valve, punctured through both surfaces twice with a 22-gauge needle. 125 mg/kg of $\beta$-glucan were dissolved in saline and subcutaneously or orally administered in a volume of 10 ml/kg (of body weight), 4 times, 12 hrs intervals from 6 hrs after CLP or 1 day after second dose of CPA. After treatment of $\beta$-glucan, the mortalities were observed in CPA-CLP model, and the appearance of a micronucleus is used as an index for genotoxic potential in CPA model. As results of CPA-CLP sepsis, all animals (9/9, 100%) in CPA-CLP control were dead within 2 days after CLP. In addition, increase of the number of bone marrow MNPCEs indicated mutagenicity were also observed by treatment of CPA. However, $\beta$-glucan treatment effectively inhibited the mortalities in CPA-CLP, and it also reduced the CPA treatment-related mutagenicity, respectively. These results indicated that $\beta$-glucan has effective anti-septic and anti-mutagenic effects and can be used as an agents for treating sepsis and mutagenicity related to high-dose chemotherapy or radiotherapy. However, further studies should be conducted to observe more detail action mechanisms of it's anti-septic and anti-mutagenic effects.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.79-81
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• 2008

The effects of decursinol on various models of sepsis were investigated. Intra-peritoneal pretreatment of mice with various doses of decursinol ($1{\sim}100$ mg/kg) effectively suppressed lethality induced in three mouse models of experimental sepsis, i.e., lipopolysaccharide (LPS)/D-galactosamine (GalN), high-dose LPS (20 mg/kg), and cecal ligation and puncture (CLP). Intra-peritoneal pretreatment of mice with decursinol (50 mg/kg) markedly enhanced the LPS/GalN -induced increase of plasma interleukin-10 (IL-10) levels, without affecting plasma TNF-${\alpha}$, IL-6 and IL-12 levels. These results suggest that decursinol could be effective for prevention or treatment of sepsis.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.301.3-302
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• 2002

Sepsis remains the leading cause of morbidity and mortality following trauma. Although hepatocellular dysfunction occurs during trauma and sepsis. the mechanism responsible for this remains unclear. We investigated the role of Kupffer cells in the alterations in microsomal drug metabolizing function during trauma and sepsis. Rats were subjected to trauma by femur fracture (FFx). After 72h, polymicrobial sepsis was induced by cecal ligation and puncture(CLP). (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.399-408
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• 2018

A lipidomic study on extensive plasma lipids in bacterial peritonitis (cecal ligation and puncture, CLP)-induced sepsis in mice was done at 24 h post-CLP. The effects of administration of lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), compounds known to have beneficial effects in CLP, on the sepsis-induced plasma lipid changes were also examined. Among the 147 plasma lipid species from 13 lipid subgroups (fatty acid [FA], LPA, LPC, lysophosphatidylethanolamine [LPE], phosphatidic acid [PA], phosphatidylcholine [PC], phosphatidylethanolamine [PE], phosphatidylinositol [PI], monoacylglyceride [MG], diacylglyceride [DG], triacylglyceride [TG], sphingomyelin [SM], and ceramide [Cer]) analyzed in this study, 40 and 70 species were increased, and decreased, respectively, in the CLP mice. Treatments with LPC and LPA affected 14 species from 7 subgroups, and 25 species from 9 subgroups, respectively. These results could contribute to finding the much needed reliable biomarkers of sepsis.

• Journal of Life Science
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• v.23 no.5
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• pp.650-656
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• 2013

Endothelial protein C receptor (EPCR) plays a pivotal role in augmenting Protein C activation through the thrombin-thrombomodulin complex. EPCR activity is markedly changed by ectodomain cleavage and released as the soluble protein (sEPCR). EPCR shedding is mediated by tumor necrosis factor-${\alpha}$ converting enzyme (TACE). Lycopene found in tomatoes and tomato products has anti-oxidant, anti- cancer and anti-inflammatory effects. However, little is known about the effects of lycopene on EPCR shedding. We investigated this issue by monitoring the effects of lycopene on the phorbol-12-myristate 13-acetate (PMA), tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$ and on the cecal ligation and puncture (CLP)-mediated EPCR shedding. Data showed that lycopene potently inhibited the PMA, TNF-${\alpha}$, IL-$1{\beta}$ and CLP-induced EPCR shedding by suppressing TACE expression. Furthermore, lycopene reduced PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2 and c-Jun N-terminal kinase (JNK). Given these results, lycopene should be viewed as a candidate therapeutic agent for the treatment of various severe vascular inflammatory diseases via inhibition of the EPCR shedding.