celecoxib

出典: meddic

セレコキシブ

WordNet   license wordnet

「a Cox-2 inhibitor (trade name Celebrex) that relieves pain and inflammation without harming the digestive tract」
Celebrex

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/04/01 10:49:38」(JST)

wiki en

[Wiki en表示]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/08/20 01:17:10」(JST)

wiki en

[Wiki en表示]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/12/16 23:57:30」(JST)

wiki en

[Wiki en表示]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/12/20 22:04:48」(JST)

wiki en

[Wiki en表示]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/11/22 10:21:38」(JST)

wiki en

[Wiki en表示]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2017/03/08 05:31:29」(JST)

wiki en

[Wiki en表示]

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

英文文献

  • Upregulation of androgen-responsive genes and transforming growth factor-β1 cascade genes in a rat model of non-bacterial prostatic inflammation.
  • Funahashi Y, O'Malley KJ, Kawamorita N, Tyagi P, Defranco DB, Takahashi R, Gotoh M, Wang Z, Yoshimura N.Author information Departments of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.AbstractBACKGROUND: Prostatic inflammation is associated with the development of prostatic hyperplasia. We investigated the effects of prostatic inflammation on expression levels of androgen-responsive genes and growth factors in the prostate.
  • The Prostate.Prostate.2014 Apr;74(4):337-45. doi: 10.1002/pros.22668. Epub 2013 Dec 17.
  • BACKGROUND: Prostatic inflammation is associated with the development of prostatic hyperplasia. We investigated the effects of prostatic inflammation on expression levels of androgen-responsive genes and growth factors in the prostate.METHODS: Prostatic inflammation was induced by formalin injection
  • PMID 24446128
  • The cytokine model of schizophrenia: emerging therapeutic strategies.
  • Girgis RR1, Kumar SS2, Brown AS3.Author information 1Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York; New York State Psychiatric Institute, New York, New York.2Department of Epidemiology, Columbia University College of Physicians and Surgeons, New York, New York; New York State Psychiatric Institute, New York, New York.3Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York; Department of Epidemiology, Columbia University College of Physicians and Surgeons, New York, New York; New York State Psychiatric Institute, New York, New York. Electronic address: asb11@columbia.edu.AbstractWe discuss the rationale for a trial of a novel biological immunotherapy in schizophrenia (SCZ). Available antipsychotic treatments for SCZ are often limited by partial effectiveness and significant side effects. The search for novel medications is of high priority. All current antipsychotics function primarily by blocking D2-type dopamine receptors. An emerging theory of SCZ postulates disturbances of cytokines and inflammatory mediators (i.e., the cytokine model), possibly originating in part from infectious exposures. Cytokines are one of the most important components of the immune system that orchestrate the response to infectious and other exogenous insults. Preclinical models of SCZ support a convergence between a role for certain cytokines in the pathophysiology of SCZ and major neurochemical postulates of the disorder, including the dopamine and glutamate hypotheses. Several cytokines are elevated in plasma in SCZ, and positron emission tomography studies have shown active inflammation in the brains of patients with psychosis. Treatment studies of anti-inflammatory agents, such as celecoxib and aspirin, in patients with SCZ have provided further support for neuroinflammation in this disorder. The development of approved biological therapies for autoimmune diseases provides new opportunities to target cytokine signaling directly as a novel treatment strategy in SCZ. In addition, advances in imaging, immunology, and psychopharmacology have paved the way for using measures of target engagement of neuroimmune components that would facilitate the identification of patient subgroups who are most likely to benefit from cytokine modulation.
  • Biological psychiatry.Biol Psychiatry.2014 Feb 15;75(4):292-9. doi: 10.1016/j.biopsych.2013.12.002. Epub 2013 Dec 11.
  • We discuss the rationale for a trial of a novel biological immunotherapy in schizophrenia (SCZ). Available antipsychotic treatments for SCZ are often limited by partial effectiveness and significant side effects. The search for novel medications is of high priority. All current antipsychotics functi
  • PMID 24439555
  • COX-2 is involved in ET-1-induced hypertrophy of neonatal rat cardiomyocytes: Role of NFATc3.
  • Li H1, Gao S1, Ye J1, Feng X1, Cai Y2, Liu Z1, Lu J1, Li Q1, Huang X1, Chen S3, Liu P4.Author information 1Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China.2Guangzhou Research Institute of Snake Venom, Guangzhou Medical College, Guangzhou 510182, Guangdong, PR China.3Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China. Electronic address: chshaor@mail.sysu.edu.cn.4Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China. Electronic address: liupq@mail.sysu.edu.cn.AbstractEndothelin-1 (ET-1) is a critical molecule that involved in heart failure. It has been proved that ET-1 stimulation results in cardiac hypertrophy both in vitro and in vivo, but the mechanisms underlying remain largely unknown. In this study, we reported that cyclooxygenase-2 (COX-2) might be an important mediator of hypertrophic responses to ET-1 stimulation. In the cultured rat neonatal cardiomyocytes, ET-1 significantly upregulated the expression and activity of COX-2, which was accompanied by increase in cell surface area and BNP mRNA level. In contrast, ET-1-dependent cardiomyocyte hypertrophy was abolished by COX-2 selective inhibitors, NS-398 and celecoxib, or by COX-2 RNA interference, but the inhibitory effects could be diminished by pretreatment with PGE2. Furthermore, cyclosporin A (CsA) and knockdown of nuclear factor of activated T-cells c3 (NFATc3) inhibited the expression of COX-2 induced by ET-1, and NFATc3 could also bound to the -GGAAA- sequence in the promoter region of rat COX-2 gene, indicating that calcineurin/NFATc3 signaling participated in the transcriptional regulation of COX-2 following ET-1 treatment. These findings provided further insight into the roles of ET-1 in cardiac hypertrophy and suggested a potential therapeutic strategy against cardiac hypertrophy by inhibiting COX-2.
  • Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Feb 15;382(2):998-1006. doi: 10.1016/j.mce.2013.11.012. Epub 2013 Nov 26.
  • Endothelin-1 (ET-1) is a critical molecule that involved in heart failure. It has been proved that ET-1 stimulation results in cardiac hypertrophy both in vitro and in vivo, but the mechanisms underlying remain largely unknown. In this study, we reported that cyclooxygenase-2 (COX-2) might be an imp
  • PMID 24291639

和文文献

  • 症例報告 セレコキシブによる薬疹の1例
  • 赤松 佳奈,角村 由紀子,日野上 はるな [他]
  • 臨床皮膚科 67(1), 17-20, 2013-01-00
  • NAID 40019558414
  • NSAIDs起因性多発小腸潰瘍から穿孔をきたした1症例
  • 竹内 庸浩,前田 哲男,多田 秀敏,西田 悠,野村 祐介,牧野 哲哉,仙波 秀峰
  • 日本消化器内視鏡学会雑誌 55(3), 467-475, 2013
  • 症例は83歳男性.黒色便を主訴に救急搬送され,下部消化管内視鏡検査にて回腸に多発潰瘍を認めた.低用量アスピリンとの関係が疑われ,内服を中止の上,絶食にて加療した.経過中,高熱,炎症反応高値を繰り返したが,内視鏡所見上,小腸潰瘍はほぼ治癒した.腰部脊柱管狭窄による腰痛のため入院第53日よりセレコキシブ200mg/日投与を開始した.入院第78日,激しい腹痛が出現し,腹部CT検査で遊離ガスを認め,消化管 …
  • NAID 130003375268
  • Successful Treatment of an Unresectable Inflammatory Myofibroblastic Tumor of the Frontal Bone Using a Cyclooxygenase-2 Inhibitor and Methotrexate
  • Kusunoki-Nakamoto Fumiko,Matsukawa Takashi,Tanaka Masaki,Miyagawa Toji,Yamamoto Tomotaka,Shimizu Jun,Ikemura Masako,Shibahara Junji,Tsuji Shoji
  • Internal Medicine 52(5), 623-628, 2013
  • Celecoxib and methotrexate were effective treatments. … Our experience suggests the efficacy of celecoxib and methotrexate as alternatives for treating unresectable IMT. …
  • NAID 130003365922

関連リンク

セレコキシブ(Celecoxib, 日本における製品名:セレコックス)は、非ステロイド性消炎・ 鎮痛薬(Non-steroidal anti-inflammatory Drugs:NSAID)であり、100mgと200mgの 錠剤がある。セレコキシブは、COX-2を選択的に阻害することを目的にドラッグデザイン ...
Celecoxib INN (/sɛlɨˈkɒksɪb/ SE-lə-KOK-sib) is a sulfonamide nonsteroidal anti-inflammatory drug (NSAID) and selective COX-2 inhibitor used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and ...

関連画像

con principio activo diferencia Celecoxib  Effects of COX-2 Inhibitors: CelecoxibCelecoxibCelecoxibCelebrex (celecoxib)CELBEXX (CELECOXIB)


★リンクテーブル★
リンク元セレコキシブ

セレコキシブ」

  [★]

celecoxib
セレコックス、Celebrex
非ステロイド性消炎鎮痛薬





★コメント★

[メモ入力エリア]
※コメント5000文字まで
ニックネーム:
コメント:




表示
個人用ツール


  meddic.jp

リンク
連絡