• 제목/요약/키워드: cecal ligation

검색결과 29건 처리시간 0.038초

맹장 결찰계(Cecal-ligated Chicken)를 이용한 [15N]urea의 이용성에 관한 연구 (A Study on the Utilization of Dietary [15N]urea in Cecal Ligated Chickens)

  • 손장호
    • 한국가금학회지
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    • 제38권1호
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    • pp.37-43
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    • 2011
  • 본 연구는 맹장 결찰계를 이용하여서 [15N]urea의 이용성을 조사하였다. 질소의 balance 및 이용률은 맹장 결찰 수술에 의해서 높아지는 경향이 인정되었다. 이는 맹장 결찰 수술로 인한 요산 배설량의 유의한 감소로 인한 결과였다(사료 및 요소 유래 질소 이용률, P<0.01). 닭에 있어서 맹장 결찰 수술은 사료 유래 ammonia 배설량은 증가(P<0.01), 요소 유래 ammonia배설량은 감소(P<0.01)시켰다. 요소 유래, 요소질소의 배설량은 맹장 결찰 수술에 의해서 유의하게 증가하였지만(P<0.01), 맹장 결찰계도 5% 단백질 사료와 같이 급여한 요소를 51.6%정도 이용하는 것으로 나타났다. 결론적으로 닭에 있어서 단백질 수준이 결핍된 사료와 같이 급여된 요소의 이용에 있어서 맹장은 유의한 역할을 한다고 할 수 있다. 하지만 질소의 이용에 있어서는 반드시 긍정적인 역할만을 한다고는 결론내릴 수 없다.

닭에 있어서 사료섭취의 자유 및 제한급여시킬 때의 사료섭취량, 음수량 및 수분 배설량에 미치는 맹장결찰 및 인공항문 수술의 효과 (Effects of Cecal Ligation and Colostomy on Food and Water Intake and loafer Excretion in Chickens Fed Restrictedly and Freely)

  • Son, J.H.
    • 한국가금학회지
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    • 제29권4호
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    • pp.259-263
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    • 2002
  • 본 연구는 닭에 있어서 맹장을 포함한 하부소화관으로 요(尿)의 역류가 음수량 및 수분 배설량에 어떠한 영향을 미칠지를 또한 사료의 섭취량이 요 (尿)의 역류량에 어떤 영향을 미칠지를 시험하였다. 급여사료를 제한 및 무제한 급여의 양조건에서 사육된 대조구 닭과 맹장이 결찰된 닭에 인공항문 수술을 실시하면 음수량, 총 수분배설량 및 음수량/사료섭취 량이 유의하게 증가(P<0.05)하였으며 이 증가량은 사료섭취 량을 무제한 급여하였을 때가 제한 급여하였을 때보다 더 크게 나타났다. 사료의 섭취량을 무제한으로 하였을 때에 대조구 닭과 인공항문이 장착된 닭에 맹장결찰 수술을 실시하면 음수량, 총 수분 배설량 및 음수량/사료섭취량이 유의하게 증가(P<0.05)하였지만, 제한급여 조건에서는 나타나지 않았다. 제한 급여 및 무제한 급여의 양 조건에서 수분균형은 인공항문 수술 및 맹장결찰 수술에 따른 변화는 나타나지 않았다. 대조구 닭과 맹장이 결찰된 닭에서의 인공항문 수술은 사료섭취 량을 증가(P<0.05)시켰지만. 대조구 닭과 인공항문이 장착된 닭에서의 맹장결찰 수술은 사료섭취량에 영향을 미치지 않았다. 이상의 결과 닭에 있어서 맹장을 포함한 하부소화관은 수분균형을 유지하기 위해서 요(尿)로부터 수분을 재 흡수하는 매우 중요한 역할을 하고 있다고 결론을 내린다.

Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis

  • Park, Donghwan;Ro, MyungJa;Lee, A-Jin;Kwak, Dong-Wook;Chung, Yunro;Kim, Jae-Hong
    • Molecules and Cells
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    • 제44권12호
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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.

Role of Kupffer Cells in Hepatic Drug Metabolizing Dysfunction during Polymicrobial Sepsis

  • Lee, Sang-Ho;Kim, Joo-Young;Eum, Hyun-Ae;Lee, Sun-Mee
    • 대한약학회:학술대회논문집
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    • 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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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)

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Berberine Prevents Intestinal Mucosal Barrier Damage During Early Phase of Sepsis in Rat through the Toll-Like Receptors Signaling Pathway

  • Li, Guo-Xun;Wang, Xi-Mo;Jiang, Tao;Gong, Jian-Feng;Niu, Ling-Ying;Li, Ning
    • The Korean Journal of Physiology and Pharmacology
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    • 제19권1호
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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.

흑효모유래 $\beta$-glucan의 패혈증 치료효과 및 항돌연변이 활성 평가 (Anti-mutagenic and Anti-septic Effects of $\beta$-glucan from Aureobasidium pullulans SM-2001)

  • 구세광
    • 한국한의학연구원논문집
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    • 제15권3호
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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.

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Protective Effect of Decursinol on Mouse Models of Sepsis: Enhancement of Interleukin-10

  • Jung, Jun-Sub;Yan, Ji-Jing;Song, Dong-Keun
    • The Korean Journal of Physiology and Pharmacology
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    • 제12권2호
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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.

Kupffer Cells Are Responsible for Producing Hepatic Microsomal Drug Metabolizing Dysfunction during Trauma and Sepsis

  • Lee, Sang-Ho;Kim, Joo-Young;Kim, Sung-Ho;Eum, Hyun-Ae;Lee, Sun-Mee
    • 대한약학회:학술대회논문집
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    • 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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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)

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Lipidomic analysis of plasma lipids composition changes in septic mice

  • Ahn, Won-Gyun;Jung, Jun-Sub;Song, Dong-Keun
    • The Korean Journal of Physiology and Pharmacology
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    • 제22권4호
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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.

In vitro와 in vivo에서 라이코펜이 EPCR 탈락에 미치는 영향 (Effects of Lycopene on Endothelial Protein C Receptor Shedding In Vitro and In Vivo)

  • 유하영;이현식;이원화;배종섭
    • 생명과학회지
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    • 제23권5호
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    • pp.650-656
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    • 2013
  • 내피세포 단백질 C 수용체(EPCR)가 트롬빈-트롬보모듈린 복합체에 의한 단백질 C (PC) 활성 증가에 중요한 역할을 한다. EPCR의 활성은 ecodomain의 분열과 수용성 단백질(sEPCR)로 분비함으로써 현저하게 변화한다. EPCR의 탈락은 tumor necrosis factor-${\alpha}$ converting enzyme (TACE)에 의해 매개된다. 토마토에서 발견된 라이코펜은 항산화 효과, 항암 효과, 항염증 효과를 가지고 있다. 그러나 EPCR 탈락에서의 라이코펜의 효과는 알려지지 않았다. 우리는 라이코펜이 PMA, TNF-${\alpha}$, IL-$1{\beta}$와 CLP에 의해 유도된 EPCR 탈락에 미치는 영향을 연구했다. 그 결과, 라이코펜은 TACE의 발현을 억제시켜 PMA, TNF-${\alpha}$, IL-$1{\beta}$와 CLP에 의해 매개된 EPCR 탈락을 저해함을 보여준다. 또한 라이코펜은 PMA가 유발한 p38, ERK1/2, JNK의 인산화를 감소시켰다. 이러한 결과를 토대로, 라이코펜은 EPCR 탈락의 저해를 통해 다양한 중증 혈관 염증 질병 치료를 위한 후보 물질이 될 수 있을 것이다.