• 제목/요약/키워드: cox3

검색결과 1,637건 처리시간 0.029초

흰쥐의 급성 십이지장 손상에 대한 반하사심탕의 방어효과에 관한 연구 (A Study on the Defence Effect of Banhasasim-tang for White Rat's Acute Duodenal Injury)

  • 한이수;최준혁;임성우
    • 대한한의학회지
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    • 제23권3호
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    • pp.188-199
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    • 2002
  • Objectives : Banhasasim-tang has been clinically used to treat upper gastric intestinal discomfort. The object of this study is to examine the defense effect of Banhasasim-tang for acute duodenal injury of the mouse. Methods and Materials : Twenty-one rats were divided into 3 groups and treated as follows: the control group was untreated mice. The ADE group was acute duodenal-damage-elicited mice. The BST group was Banhasasim-tang treated mice before acute duodenal damage elicitation. The groups were examined with common morphology, paneth cells in intestinal crypt, absorptive cells and goblet cells in epithelium, cell division in mucose, COX-l as mucosal protector, COX-2 (which appears to play an important role in inflammation), IL-2R-inducing cellular immuno-chainreaction, and the distribution of apoptotic cells. Results : 1. Common morphology: the ADE group was observed with duodenal injury - loss of villi, infiltration of cells concerned to inflammation (lymphocytes, granular leukocytes) to submucosal layer - by hemorrhagic erosions, while the BST group was seen the same as normal in proportion to increasing treatment time before injury. 2. Histochemical change: the ADE group was observed with noticeable decreased distribution of absorptive cells with microvilli, acid mucin secreted goblet cell, neutral mucin secreted goblet cell, paneth cells compared to the normal group. The BST group was seen to have distribution of epithelium cells resembling normal in proportion to increasing treatment time before injury. 3. Imnunohistochemical change: the ADE group showed a change of factors leading to duodenal injury as reduce of cytokinesis, COX-1, increase of COX-2, IL-2R-. In contrast, the BST group tended to reduction of cytokinesis, COX-1, increase of COX-2, IL-2R- in proportion to increasing taking time before injury. 4. Apoptosis change: the ADE group showed increasing apoptosis cells, in contrast to the BST group which was the same as normal in proportion to increasing treatment time before injury. Conclusions : According to the above results, by increasing the defense system of mucosal epithelium, Banhasasim-tang is thought to effectively protect tissue against ulcers resulting from acute duodenal injury.

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Neuroprotective Effect of N-nitro-L-arginine Methylester Pretreatment on the Early Stage of Kainic Acid Induced Neuronal Degeneration in the Rat Brain

  • Koh, Jun-Seok;Kim, Gook-Ki;Lim, Young-Jin;Rhee, Bong-Arm;Kim, Tae-Sung
    • Journal of Korean Neurosurgical Society
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    • 제38권4호
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    • pp.287-292
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    • 2005
  • Objective : Kainic acid[KA] enhances the expression of nitric oxide synthase, increases nitric oxide[NO], and thus evokes epileptic convulsion, which results in neuronal damage in the rat brain. NO may stimulate cyclooxygenase type-2 [COX-2] activity, thus producing seizure and neuronal injury, but it has also been reported that KA-induced seizure and neurodegeneration are aggravated on decreasing the COX-2 level. This study was undertaken to investigate whether the suppression of NO using the NOS inhibitor, N-nitro-L-arginine methyl ester[L-NAME], suppresses or enhances the activity of COX-2. Methods : Silver impregnation and COX-2 immunohistochemical staining were used to localize related pathophysiological processes in the rat forebrain following KA-induced epileptic convulsion and L-NAME pretreatment. Post-injection survival of the rat was 1, 2, 3days and 2months, respectively. Results : After the systemic administration of KA in rats, neurodegeneration increased with time in the cornu ammonis [CA] 3, CA 1 and amygdala, as confirmed by silver impregnation. On pretreating L-NAME, KA-induced neuronal degeneration decreased. COX-2 enzyme activities increased after KA injection in the dentate gyrus, CA 3, CA 1, amygdala and pyriform cortex, as determined by COX-2 staining. L-NAME pretreatment prior to KA-injection, caused COX-2 activities to increase compared with KA- injection only group by 1day and 2days survival time point. Conclusion : These results suggest that L-NAME has a neuroprotective effect on KA-induced neuronal damage, especially during the early stage of neurodegeneration.

Inhibition of COX-2 Activity and Proinflammatory Cytokines($TNF-{\alpha}{\;}and{\;}IL-1{\beta}$) Production by Water-Soluble Sub-Fractionated Parts from Bee (Apis mellifera) Venom

  • Nam, Kung-Woo;Je, Kang-Hoon;Lee, Jang-Hurn;Han, Ho-Je;Lee, Hye-Jung;Kang, Sung-Kil;Mar, Woongchon
    • Archives of Pharmacal Research
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    • 제26권5호
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    • pp.383-388
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    • 2003
  • Bee venom is used as a traditional medicine for treatment of arthritis. The anti-inflammatory activity of the n-hexane, ethyl acetate, and aqueous partitions from bee venom (Apis mellifera) was studied using cyclooxygenase (COX) activity and pro-inflammatory cytokines (TNF-$\alpha and IL-1\beta$) production, in vitro. COX-2 is involved in the production of prostaglandins that mediate pain and support the inflammatory process. The aqueous partition of bee venom showed strong dose-dependent inhibitory effects on COX-2 activity ($IC_{50} = 13.1 \mu$ g/mL), but did not inhibit COX-1 activity. The aqueous partition was subfractionated into three parts by molecular weight differences, namely, B-F1 (above 20 KDa), B-F2 (between 10 KDa and 20 KDa) and BF-3 (below 10 KDa). B-F2 and B-F3 strongly inhibited COX-2 activity and COX-2 mRNA expression in a dose-dependent manner, without revealing cytotoxic effects. TNF-$\alpha and IL-1\beta$ are potent pro-inflammatory cytokines and are early indicators of the inflammatory process. We also investigated the effects of three subfractions on TNF-$\alpha and IL-1\beta$ production using ELISA method. All three subfractions, B-F1, B-F2 and B-F3, inhibited TNF-$\alpha and IL-1\beta$production. These results suggest the pharmacological activities of bee venom on anti-inflammatory process include the inhibition of COX-2 expression and the blocking of pro-inflammatory cytokines (TNF-$\alpha and IL-1\beta$) production.

A STUDY ON THE EFFECT OF POWER TRANSFORMATION IN SPATIAL STATISTIC ANALYSIS

  • LEE JIN-HEE;SHIN KEY-IL
    • Journal of the Korean Statistical Society
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    • 제34권3호
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    • pp.173-183
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    • 2005
  • The Box-Cox power transformation is generally used for variance stabilization. Recently, Shin and Kang (2001) showed, under the Box-Cox transformation, invariant properties to the original model under the large mean and relatively small variance assumptions in time series analysis. In this paper we obtain some invariant properties in spatial statistics. Spatial statistics, Invariant Property, Variogram, Box-Cox power Transformation.

Cox proportional hazard model with L1 penalty

  • Hwang, Chang-Ha;Shim, Joo-Yong
    • Journal of the Korean Data and Information Science Society
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    • 제22권3호
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    • pp.613-618
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    • 2011
  • The proposed method is based on a penalized log partial likelihood of Cox proportional hazard model with L1-penalty. We use the iteratively reweighted least squares procedure to solve L1 penalized log partial likelihood function of Cox proportional hazard model. It provide the ecient computation including variable selection and leads to the generalized cross validation function for the model selection. Experimental results are then presented to indicate the performance of the proposed procedure.

고혈압 관련 측면에서의 alphaENaC, ET-1, cox-2 유전자의 소금에 의한 조절 기전 (Sodium Chloride Regulation of $\alpha$ENaC, ET-1, and COX-2 Genes: A Possible Implication of Hypertension)

  • Lee, Young-Joo
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 2003년도 춘계학술대회
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    • pp.113-130
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    • 2003
  • 1. We have established a model system to study sodium chloride, an environmental factor, induced gene regulations. 2. ${\alpha}$ENaC, cox-2, and c-fos genes are regulated by sodium chloride at mRNA level as well as at protein level. 3. Regulation of ${\alpha}$ENaC requires syntheses of new protein(s). 4. COX-2 may have a important role for homeostasis in hypertonic situation.

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CELECOXIB ATTENUATES ET-18-O-CH3-INDUCED APOPTOSIS IN H-ras TRANSFORMED HUMAN BREAST EPITHELIAL CELLS

  • Na, Hye-Kyung;Surh, Young-Joon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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    • pp.154-155
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    • 2001
  • Cyclooxygenase-2 (COX-2) is an inducible enzyme expressed in response to a variety of proinflammatory agents and cytokines. COX-2 expression has been shown to be elevated in several different types of human cancer. The presence of oncogenic ras has been associated with constitutive induction of COX-2 in certain H-ras transformed cells, and COX-2 overexpression confers resistance to apoptosis.(omitted)

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승모판막질환을 동반하지 않은 심방세동에서의 Cox-Maze 술식 -3례 보고- (The Cox-Maze Procedure for Atrial Fibrillation not Associated with Mitral Valve Disease -Report of three cases-)

  • 강창현;김기봉
    • Journal of Chest Surgery
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    • 제31권12호
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    • pp.1230-1233
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    • 1998
  • The Cox-Maze procedure was developed as a cure for atrial fibrillation. The recovery rate of both atrial contractility is reported low in the atrial fibrillation associated with mitral valvular heart disease than that of loan atrial fibrillation. We performed the Cox-Maze procedure (Maze III) in three cases who suffered from non-mitral heart diseases associated with atrial fibrillation: A ruptured sinus of Valsalva aneurysm, a ventricular septal defect, and an aortic stenoinsufficiency. The Cox-Maze procedure was performed concomitantly with correction of the underlying heart disease. Conversion to sinus rhythm was achieved in all three patients, and both right and left atrial mechanical activities could be identified echocardiographically after three postoperative months.

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COX 억제제에 의해 유도되는 구강편평세포암종 세포주의 성장 억제 효과 (GROWTH INHIBITION OF ORAL SQUAMOUS CELL CARCINORMA CELL LINE INDUCED BY COX INHIBITOR)

  • 박광진;한세진;이재훈
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제30권4호
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    • pp.333-344
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    • 2008
  • The objectives of this study was to explore the growth pattern of the oral squamous cell carcinoma when overexpressed COX was inhibited, explore the pathway that COX inhibitors suppressed the proliferation of cancer cells, and then hereafter investigate the potential of COX as chemopreventive target for oral squamous cell carcinoma. For confirming the COX-dependent effect and mechanisms on growth of the oral cancer cells, we treated the nonselective NSAID, Mefenamic acid and COX-2 selective inhibitor, Celecoxib in HN4 cell line. And then the cell line was evaluated with MTT assay and growth curve, the production of PGE2, total RNA extraction and RT-PCR analysis, and TEM The results were obtained as follows: 1. After administration of medication, in the result of MTT assay, Celecoxib inoculated group inhibit the cell growth rather than Mefenamic acid inoculated group. 2. The growth curve of cell line showed as time passes by there was a dramatic cell growth in the control group, and gradual growth inhibition was found in medication inoculated group and, in Celecoxib inoculated group there was more inhibition of cell growth. 3. After the administration of medication, Celecoxib tend to inhibit the synthesis of PGE2 more than Mefenamic acid. Mefenamic acid inhibit the synthesis of PGE2 more as the concentration gets high, but Celecoxib inhibited the synthesis of PGE2 even in low concentration. 4. After the administration of medication, the revelation of COX mRNA in cell line, there was a 50% decrease in COX-1, 60% decrease in COX-2 as in $50{\mu}M$ Mefenamic acid, and in Celecoxib $50{\mu}M$ there was not much difference in COX-1 and 90% decrease in COX-2 was found. 5. HN4 cell line showed broken nucleus and tangled cytoskeleton bundles in cytoplasm which meant apoptotic features after the treatment of Celecoxib in TEM view. Depending on the above results, we estimate that the inhibition of the expression of COX-2 cause the growth suppression of the oral squamous cell carcinoma, and it get achieved through pathway of reduced PGE2 production and increased apoptosis. In addition to, because COX-2 selective inhibitor specifically act to COX-2, it is considered that COX-2 selective inhibitor has the adequate potential as chemopreventive agent for oral squamous cell carcinoma.

양성 및 악성 연골 종양의 Cyclooxygenase-2 발현 (Cyclooxygenase-2 Expression in Benign and Malignant Chondroid Tumors)

  • 박혜림;민광선;박용구
    • 대한골관절종양학회지
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    • 제13권2호
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    • pp.105-112
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    • 2007
  • 목적: 최근 골 및 연부조직 종양을 포함한 각종 악성 종양에서 cyclooxygenase-2 (COX-2) 의 발현 증가가 보고되고 있다. 그러나 연골 종양에서의 COX-2 발현에 대해서는 별로 알려진 바가 없다. 대상 및 방법: 내연골종 10예, 연골모세포종 11예, 연골점액양섬유종 5예, 통상적 연골육종 17예, 투명세포 연골육종 7예, 간엽성 연골육종 6예를 대상으로 COX-2에 대한 면역조직화학법을 시행하였다. 결과: 양성 연골 종양 중 연골모세포종 11예 중 6예(54.5%)에서 특징적인 강한 양성 반응을 나타내었다. 내연골종과 연골점액양섬유종은 단 1예를 제외하고는 모든 증례에서 음성이었다. 통상적인 연골육종에서 3예(17.6%)는 COX-2에 대해 강한 양성 반응을 보였는데 이러한 양성 증례는 모두 조직학적 등급 3의 분화가 나쁜 연골육종이었다. 투명세포 연골육종 중 2예(28.5%)는 국소적인 양성 반응을 나타내었고 모든 간엽성 연골육종은 음성이었다. 결론: 이러한 결과는 통상적인 연골육종에서 COX-2 과발현이 조직학적 등급 진행과 관계된 소견임을 시사한다. 연골모세포종의 COX-2 발현은 특별히 이 종양에 동반되는 종양 주변부의 염증성 변화를 유발하는 중요한 요소로 생각된다.

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