• 제목/요약/키워드: Selective inhibitor

검색결과 399건 처리시간 0.024초

DEPRENYL INHIBITS POTENTIATED ARSENIC-INDUCED CYTOTOXICITY VIA THE INHIBITION OF C-JUN N- TERMINAL KINASE ACTIVATION

  • Park, Jeong-Weon;Kim, Sang-Geon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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    • pp.147-147
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    • 2001
  • A previous study showed that sulfur amino acid deprivation (SAAD) potentiated cytotoxicity induced by arsenic (As) and that activation of ERKl/2, p38 kinase and JNK1 was responsible for the potentiation of As toxicity. In the present study, we found for the first time that deprenyl a selective monoamine oxidase B inhibitor prevented potentiation of As toxicity by SAAD in a dose-dependent manner.(omitted)

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Oral Efficacy of DA-8159, a Novel Selective PDE 5 Inhibitor, for Inducing Penile Erection in Conscious Rabbits

  • Kang, Kyung-Koo;Oh, Tae-Young;Choi, Seul-Min;Kim, Ju-Mi;Ahn, Byoung-Ok;Kwon, Jong-Won;Kim, Won-Baw
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 2002년도 창립10주년기념 및 국립독성연구원 의약품동등성평가부서 신설기념 국재학술대회:생물학적 동등성과 의약품 개발 전략을 위한 국제심포지움
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    • pp.232-232
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    • 2002
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CELECOXIB INHIBITS PHORBOL ESTER-INDUCED PGE$_2$ PRODUCTION AND COX-2 EXPRESSION BY TARGETING OF p38 MAP KINASE AND AP-1 IN MOUSE SKIN

  • Chun, Kyung-Soo;Surh, Young-Joon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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    • pp.175-175
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    • 2002
  • Celecoxib, a selective COX-2 inhibitor, has been reported to prevent experimentally induced colon, breast, bladder, and skin carcinogenesis. Moreover, daily intake of celecoxib resulted in significant reduction of polyps in patients with familial adenomatous polyposis.(omitted)

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Solution-Phase Strategies for the Design, Synthesis, and Screening of Libraries Based on Natural Products

  • Kim, Sang-Hee
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-1
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    • pp.88-88
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    • 2003
  • The syntheses of different types of stilbenoid libraries have been studied recently. In these courses, the screening of the generated natural product-mimic focused libraries led to the identification of the novel lead compounds for human cytochrome P450 (CYP) lAs, melanin production, and sortase A. A library of trans-stilbene derivatives was prepared through a new efficient solution pahse synthetic pathway and their inhibitory activities were evaluated on human cytochrome P450s(CYP) 1A1, 1A2, and 1B1 to find a potent and selective CYP1 inhibitor. (omitted)

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Depression, what should we be doing?

  • Ko, Kyung-Ja;Kim, Hyung-Min
    • 셀메드
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    • 제9권2호
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    • pp.2.1-2.1
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    • 2019
  • Depression is common psychiatric diseases characterized by diverse physical and emotional symptoms including low mood, loss of interest in pleasurable activities, and feelings of worthlessness. Depression causes of death and disability. The first antidepressant was created by the idea that central serotonin mechanism. Selective serotonin reuptake inhibitor, fluoxetine is the first-line drug in the treatment of depressive disorder and their few side effects as opposed to tricyclic antidepressants. Not all people with depression respond adequately to standard treatments. Korean music playing/listening actions appear to be a reliable approach to developing recovery from depression.

Growth inhibition and cell cycle phase-specific apoptosis induced by celecoxib in human NSCLC cells in vitro.

  • Choi, Kang-Eun;Kang, Jin-Hyoung;Kuh, Hyo-Jeong
    • 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.244.1-244.1
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    • 2002
  • Cyclooxygenase-2 ( COX-2 ) is an inducible enzyme which produces prostanoids by various stimuli. Overexpression of COX-2 in many tumor types indicates its association with tumor progression, which has been a promising target for chemoprevention and chemomodulation. We studied conc- and time-dependency of COX-2 inhibition, growth inhibition, and cell cycle arrest induced by celecoxib, a selective COX-2 inhibitor, in human non-small cell lung cancer (NSCLC) A549 cells. (omitted)

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노인 우울증 환자에서 선택적 세로토닌 재흡수 억제제, 세로토닌 노르에피네프린 재흡수 억제제가 우울증상, 통증 그리고 신체증상에 미치는 효과 비교 (Comparison of Effect of SSRIs and SNRIs on Depression, Pain and Somatic Symptoms in Elderly Patients with Major Depressive Disorder)

  • 한은희;김현;이강준
    • 정신신체의학
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    • 제28권1호
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    • pp.72-80
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    • 2020
  • 연구목적 본 연구는 통증 및 신체증상이 동반된 노인 우울증 환자에서 기분증상 및 통증, 신체 증상에 대한 선택적 세로토닌 재흡수 억제제(Selective Serotonin Reuptake Inhibitor, SSRI)와 세로토닌 노르에피네프린 재흡수 억제제(Serotonin Norepinephrine Reuptake Inhibitor, SNRI)의 치료 효과를 비교하기 위해 실시되었다. 방 법 본 연구는 단일 기관에서 시행된 전향적 개방연구로 DSM-5 진단기준에 의해 주요우울장애로 진단받은 총 43명의 대상자들이 본 연구에 참여하였다(평균연령 : 72.53세, 여성 58.1%). 대상군은 SSRI, SNRI 두 군으로 분류되었고 우울, 통증 및 신체증상은 각각 한국판 해밀턴 우울증 평가척도(Korean version of the Hamilton Depression Rating Scale, K-HDRS), 시각적 비율 척도(Visual Analogue Scale, VAS), 환자 건강 설문지(Patient Health Questionnare-15, PHQ-15)를 사용하여 평가되었다. 이원배치 반복측정 분산분석(Two-way repeated-measure ANOVA)으로 약물 투여 전과 투여 후 6주의 KHDRS, VAS, PHQ-15 점수 변화를 분석하였다. 결 과 SSRI군과 SNRI군에서 K-HDRS, VAS, PHQ-15 모두 약물 투약 전에 비해 6주 후의 점수가 유의하게 호전되었으며, 두 군 간에 호전 정도의 차이는 없었다. 결 론 노인 우울증 환자에서 SSRI, SNRI 모두 통증 및 신체증상을 호전시키는 것으로 나타났다. 본 연구 결과는 통증 및 신체증상을 호소하는 노인 우울증 환자에게 약물치료를 시행할 때 선택할 수 있는 항우울제 처방 결정에 도움을 줄 수 있을 것이라고 생각되며, 약물의 장기적인 효과에 대해서 추가적인 연구가 필요할 것으로 보인다.

Heat shock protein 90 inhibitor AUY922 attenuates platelet-derived growth factor-BB-induced migration and proliferation of vascular smooth muscle cells

  • Kim, Jisu;Lee, Kang Pa;Kim, Bom Sahn;Lee, Sang Ju;Moon, Byung Seok;Baek, Suji
    • The Korean Journal of Physiology and Pharmacology
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    • 제24권3호
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    • pp.241-248
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    • 2020
  • Luminespib (AUY922), a heat shock proteins 90 inhibitor, has anti-neoplastic and antitumor effects. However, it is not clear whether AUY922 affects events in vascular diseases. We investigated the effects of AUY922 on the platelet-derived growth factor (PDGF)-BB-stimulated proliferation and migration of vascular smooth muscle cells (VSMC). VSMC viability was detected using the XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) reagent. To detect the attenuating effects of AUY922 on PDGF-BB-induced VSMCs migration in vitro, we performed the Boyden chamber and scratch wound healing assays. To identify AUY922-mediated changes in the signaling pathway, the phosphorylation of protein kinase B (Akt) and extracellular signal-regulated kinase (ERK) 1/2 was analyzed by immunoblotting. The inhibitory effects of AUY922 on migration and proliferation ex vivo were tested using an aortic ring assay. AUY922 was not cytotoxic at concentrations up to 5 nM. PDGF-BB-induced VSMC proliferation, migration, and sprout outgrowth were significantly decreased by AUY922 in a dose-dependent manner. AUY922 significantly reduced the PDGF-BB-stimulated phosphorylation of Akt and ERK1/2. Furthermore, PD98059 (a selective ERK1/2 inhibitor) and LY294002 (a selective Akt inhibitor) decreased VSMC migration and proliferation by inhibiting phosphorylation of Akt and ERK1/2. Greater attenuation of PDGF-BB-induced cell viability and migration was observed upon treatment with PD98059 or LY294002 in combination with AUY922. AUY922 showed anti-proliferation and anti-migration effects towards PDGF-BB-induced VSMCs by regulating the phosphorylation of ERK1/2 and Akt. Thus, AUY922 is a candidate for the treatment of atherosclerosis and restenosis.

Escitalopram, a selective serotonin reuptake inhibitor, inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells

  • Kim, Han Sol;Li, Hongliang;Kim, Hye Won;Shin, Sung Eun;Seo, Mi Seon;An, Jin Ryeol;Ha, Kwon-Soo;Han, Eun-Taek;Hong, Seok-Ho;Choi, Il-Whan;Choi, Grace;Lee, Dae-sung;Park, Won Sun
    • The Korean Journal of Physiology and Pharmacology
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    • 제21권4호
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    • pp.415-421
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    • 2017
  • We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent $K^+$ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The $IC_{50}$ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were $9.54{\pm}1.33{\mu}M$ and $0.75{\pm}0.10$, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.

Compound IKD-8344, a Selective Growth Inhibitor Against the Mycelial Form of Candida albicans, Isolated from Streptomyces sp. A6792

  • HWANG EUI IL;YUN BONG SIK;YEO WOON HYUNG;LEE SANG HAN;MOON JAE SUN;KIM YOUNG KOOK;LIM SE JIN;KIM SUNG UK
    • Journal of Microbiology and Biotechnology
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    • 제15권4호
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    • pp.909-912
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    • 2005
  • In the course of screening for selective growth inhibitors against the mycelial form of Candida albicans, we isolated a Streptomyces sp. A6792 from soils. The inhibitor was isolated from the above bacterium and identified through several spectral analyses with UV and mass spectrophotometries, and various NMR. The compound was determined to be a macrocyclic dilactone antibiotic, IKD-8344 (molecular weight: 844, molecular formula: $C_{48}H_{76}O_{12}$). The compound selectively inhibited the growth of mycelial form of C. albicans with an MIC of 6.25 ${\mu}g/ml$. It also exhibited strong inhibitory effect preferentially on the mycelial form of various Candida spp. including C. krusei, C. tropicalis, and C. lusitaniae, with MICs ranging from 1.56 to 25 ${\mu}g$/ml. Furthermore, the compound showed no significant toxicity against SPF ICR mice up to 60 mg/kg. These results suggest that IKD-8344 is a useful lead compound for the development of novel antifungal agents, based on the preferential growth inhibition against Candida spp.