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[PMID]:28603125
[Au] Autor:Adel-Kader MS; Alwahebi NWH; Alam P
[Ad] Endereço:Department of Pharmacognosy, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia / Department of Pharmacognosy, College of Pharmacy, Alexandria University, Alexandria, Egypt.
[Ti] Título:Estimation of yohimbine base in complex mixtures by quantitative HPTLC application.
[So] Source:Pak J Pharm Sci;30(1):149-154, 2017 Jan.
[Is] ISSN:1011-601X
[Cp] País de publicação:Pakistan
[La] Idioma:eng
[Ab] Resumo:The indole alkaloid Yohimbine has been used for over two centuries in the treatment of erectly dysfunction. Several formulations containing yohimbine salts, yohimbe bark power or extract are marketed worldwide. Determination of the amount of yohimbine in such formulation is a challenging task due to their complex nature. Extraction followed by acid-base purification resulted in a relatively pure alkaloids containing fractions. The exact amounts of yohimbine free base in different formulations were determined by densitometric HPTLC validated methods using silica gel TLC plates. Standard curve for yohimbine was generated using yohimbine hydrochloride subjected to the same acid-base treatment as the used samples. All formulations found to contain yohimbine though some with less concentration than the labeled amount.
[Mh] Termos MeSH primário: Antagonistas de Receptores Adrenérgicos alfa 2/análise
Cromatografia em Camada Delgada/métodos
Tecnologia Farmacêutica/métodos
Ioimbina/análise
[Mh] Termos MeSH secundário: Calibragem
Cromatografia em Camada Delgada/normas
Densitometria
Formas de Dosagem
Composição de Medicamentos
Limite de Detecção
Modelos Lineares
Padrões de Referência
Reprodutibilidade dos Testes
Sílica Gel/química
Tecnologia Farmacêutica/normas
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Antagonists); 0 (Dosage Forms); 2Y49VWD90Q (Yohimbine); 60650-90-0 (Silica Gel)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


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[PMID]:28315642
[Au] Autor:Janssen CF; Maiello P; Wright MJ; Kracinovsky KB; Newsome JT
[Ad] Endereço:Division of Laboratory Animal Resources, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, Center for Laboratory Animal Medicine and Care, University of Texas Health Science Center at Houston, Houston, Texas;, Email: Christopher.F.Janssen@uth.tmc.edu.
[Ti] Título:Comparison of Atipamezole with Yohimbine for Antagonism of Xylazine in Mice Anesthetized with Ketamine and Xylazine.
[So] Source:J Am Assoc Lab Anim Sci;56(2):142-147, 2017 Mar 01.
[Is] ISSN:1559-6109
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The α2 adrenergic agonist xylazine produces a sedative effect and is typically combined with ketamine and used for anesthesia or chemical restraint of laboratory mice. Xylazine's sedative effect-and its undesirable side effects of bradycardia, hypotension, and poor tissue perfusion-can be reversed by administration of α2 antagonists, such as atipamezole or yohimbine. Although atipamezole and yohimbine dosing guidelines are available for mice, no controlled comparison has been performed to guide the lab animal community in the selection of one over the other. This study is a single-dose crossover comparison of these 2 antagonist drugs, given intraperitoneally at clinically recommended doses, to determine which results in more rapid recovery of mice from xylazine-ketamine anesthesia. Time to return of righting reflex was used as the primary outcome measure. Mice were anesthetized with xylazine (10 mg/kg IP) and ketamine (80 mg/kg IP), followed 15 min later by injection of an α2 antagonist or saline (control). Time to return of righting reflex differed significantly among groups, with mice recovering in an average of 10.3 min after administration of atipamezole (1 mg/kg IP) as compared with 21.3 min after yohimbine (1.5 mg/kg IP) and 38.2 min after saline. When rapid recovery of mice after xylazine-ketamine anesthesia is desirable, administration of an antagonist to reverse the effects of the xylazine is indicated. When injection of the antagonist by the technically simple intraperitoneal route is desirable, our data indicate that (at the doses evaluated) atipamezole is more effective than yohimbine.
[Mh] Termos MeSH primário: Imidazóis/farmacologia
Ketamina/farmacologia
Xilazina/farmacologia
Ioimbina/farmacologia
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 2/administração & dosagem
Antagonistas de Receptores Adrenérgicos alfa 2/farmacologia
Analgésicos/administração & dosagem
Analgésicos/farmacologia
Anestesia
Animais
Estudos Cross-Over
Imidazóis/administração & dosagem
Ketamina/administração & dosagem
Ciência dos Animais de Laboratório
Masculino
Camundongos
Xilazina/administração & dosagem
Ioimbina/administração & dosagem
[Pt] Tipo de publicação:CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Antagonists); 0 (Analgesics); 0 (Imidazoles); 03N9U5JAF6 (atipamezole); 2KFG9TP5V8 (Xylazine); 2Y49VWD90Q (Yohimbine); 690G0D6V8H (Ketamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE


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[PMID]:28233634
[Au] Autor:Sasaki-Hamada S; Suzuki A; Ueda Y; Matsumoto K; Oka JI
[Ad] Endereço:Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Japan.
[Ti] Título:Serotonergic and dopaminergic systems are implicated in antidepressant-like effects of chotosan, a Kampo formula, in mice.
[So] Source:J Pharmacol Sci;133(2):110-113, 2017 Feb.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We previously demonstrated that chotosan (CTS), a traditional herbal formula called Kampo medicine, improves diabetes-induced cognitive deficits. In the present study, we investigated the antidepressant-like effects of CTS in mice. The administration of CTS (1.0 g/kg, for 3 days) decreased the immobility time in the forced-swim test, and this decrease was prevented by the prior administration of sulpiride (an antagonist of D receptors) and WAY100635 (an antagonist of 5-HT receptors). None of the treatments tested altered the locomotor activity of mice. These results suggest that CTS exerts antidepressant-like effects through changes in the serotonergic and dopaminergic systems.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Dopaminérgicos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Medicina Kampo
Serotoninérgicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Fenclonina/química
Imipramina/química
Imipramina/farmacologia
Ketanserina/química
Ketanserina/farmacologia
Locomoção
Masculino
Metergolina/química
Camundongos
Piperazinas/química
Piperazinas/farmacologia
Piridinas/química
Piridinas/farmacologia
Sulpirida/química
Sulpirida/farmacologia
Natação
Ioimbina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Dopamine Agents); 0 (Drugs, Chinese Herbal); 0 (Piperazines); 0 (Pyridines); 0 (Serotonin Agents); 0 (choto-san); 1501393LY5 (Metergoline); 2Y49VWD90Q (Yohimbine); 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide); 7MNE9M8287 (Sulpiride); 97F9DE4CT4 (Ketanserin); OGG85SX4E4 (Imipramine); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE


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[PMID]:28219708
[Au] Autor:Angus JA; Rajasekaran P; Wright CE
[Ad] Endereço:Cardiovascular Therapeutics Unit, Department of Pharmacology and Therapeutics, University of Melbourne, Victoria 3010, Australia. Electronic address: jamesaa@unimelb.edu.au.
[Ti] Título:Novel technique to determine the pK of clonidine at prejunctional α -adrenoceptors in cardiac and vascular sympathetic transmission.
[So] Source:Eur J Pharmacol;800:81-95, 2017 Apr 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Analytical pharmacology draws heavily on the concept of equilibrium of agonist and silent antagonist concentrations competing at a specific receptor site. This condition breaks down in nerve transmission when transmitter release is inhibited by prejunctional α -adrenoceptors activated by an agonist such as clonidine. We have developed a method that allows the agonist dissociation constant K of clonidine to be determined in a robust isolated right atrial assay of mouse, rat and guinea pig. By applying low numbers of field pulses 1-4 to prevent autoinhibitory feedback, clonidine shifted the nerve pulse stimulation-tachycardia curves to the right. These peak responses to field pulses were equated to responses to exogenous noradrenaline and the pK determined by global fitting and display in the Clark plot. The pK for clonidine ranged from 8.95 in the mouse, 7.8 in rat and 8.3 in guinea pig. The propranolol pK was 8.87 in mouse and 8.91 in rat atria, reading very similarly to those values from ß-adrenoceptor agonist assays under equilibrium conditions. In mesenteric resistance arteries mounted in a myograph for electrical field stimulation, clonidine again inhibited contractions to field pulses in mouse arteries with a pK of 7.12, but was inactive in rat arteries due to competing autoinhibitory feedback from nerve-released noradrenaline. In both species, prazosin inhibited the field pulses with a pK of 9.08 in rat and 9.03 in mouse arteries. We conclude that pK for antagonists and pK for the prejunctional inhibitors of nerve transmission can be determined with this novel analytical approach.
[Mh] Termos MeSH primário: Clonidina/farmacologia
Átrios do Coração/inervação
Artérias Mesentéricas/inervação
Receptores Adrenérgicos alfa 2/metabolismo
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/fisiologia
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cistamina/análogos & derivados
Cistamina/farmacologia
Desipramina/farmacologia
Relação Dose-Resposta a Droga
Cobaias
Átrios do Coração/efeitos dos fármacos
Masculino
Artérias Mesentéricas/efeitos dos fármacos
Camundongos
Norepinefrina/farmacologia
Ratos
Ioimbina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Adrenergic, alpha-2); 2Y49VWD90Q (Yohimbine); 69790-18-7 (benextramine); MN3L5RMN02 (Clonidine); R110LV8L02 (Cystamine); TG537D343B (Desipramine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE


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[PMID]:27939824
[Au] Autor:Yu Z; Saito H; Otsuka H; Shikama Y; Funayama H; Sakai M; Murai S; Nakamura M; Yokochi T; Takada H; Sugawara S; Endo Y
[Ad] Endereço:Division of Molecular Regulation, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan; Department of Disaster Psychiatry, International Research Institute for Disaster Science, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Electro
[Ti] Título:Pulmonary platelet accumulation induced by catecholamines: Its involvement in lipopolysaccharide-induced anaphylaxis-like shock.
[So] Source:Int Immunopharmacol;43:40-52, 2017 Feb.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Intravenously injected lipopolysaccharides (LPS) rapidly induce pulmonary platelet accumulation (PPA) and anaphylaxis-like shock (ALS) in mice. Macrophages reportedly release catecholamines rapidly upon stimulation with LPS. Here, we examined the involvement of macrophage-derived catecholamines in LPS-induced PPA and ALS. A catecholamine or Klebsiella O3 (KO3) LPS was intravenously injected into mice, with 5-hydroxytryptamine in the lung being measured as a platelet marker. The tested catecholamines induced PPA, leading to shock. Their minimum shock-inducing doses were at the nmol/kg level. The effects of epinephrine and norepinephrine were inhibited by prazosin (α1 antagonist) and by yohimbine (α2 antagonist), while dopamine's were inhibited only by prazosin. Use of synthetic adrenergic α1- and/or α2-agonists, platelet- or macrophage-depleted mice, a complement C5 inhibitor and C5-deficient mice revealed that (a) α2-receptor-mediated PPA and shock depend on both macrophages and complements, while α1-receptor-mediated PPA and shock depend on neither macrophages nor complements, (b) the PPA and ALS induced by KO3-LPS depend on α1- and α2-receptors, macrophages, and complements, and (c) KO3-LPS-induced PPA is preceded by catecholamines decreasing in serum. Together, these results suggest the following. (i) Catecholamines may stimulate macrophages and release complement C5 via α2-receptors. (ii) Macrophage-derived catecholamines may mediate LPS-induced PPA and ALS. (iii) Moderate PPA may serve as a defense mechanism to remove excess catecholamines from the circulation by promoting their rapid uptake, thus preventing excessive systemic effects. (iv) The present findings might provide an insight into possible future pharmacological strategies against such diseases as shock and acute respiratory distress syndrome.
[Mh] Termos MeSH primário: Anafilaxia/tratamento farmacológico
Plaquetas/efeitos dos fármacos
Catecolaminas/farmacologia
Pulmão/patologia
Macrófagos/efeitos dos fármacos
Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico
[Mh] Termos MeSH secundário: Anafilaxia/induzido quimicamente
Animais
Plaquetas/fisiologia
Células Cultivadas
Complemento C5/genética
Complemento C5/metabolismo
Seres Humanos
Lipopolissacarídeos/imunologia
Pulmão/efeitos dos fármacos
Macrófagos/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Prazosina/farmacologia
Serotonina/metabolismo
Ioimbina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (Complement C5); 0 (Lipopolysaccharides); 2Y49VWD90Q (Yohimbine); 333DO1RDJY (Serotonin); XM03YJ541D (Prazosin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


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[PMID]:27871896
[Au] Autor:de Lacerda Neto LJ; Ramos AG; Santos Sales V; de Souza SD; Dos Santos AT; de Oliveira LR; Kerntopf MR; de Albuquerque TR; Coutinho HD; Quintans-Júnior LJ; Wanderley AG; de Menezes IR
[Ad] Endereço:Chemical-Biology Department, Regional University of Cariri - URCA, Cel. Antonio Luis 1161, Crato, CE, Brazil.
[Ti] Título:Gastroprotective and ulcer healing effects of hydroethanolic extract of leaves of Caryocar coriaceum: Mechanisms involved in the gastroprotective activity.
[So] Source:Chem Biol Interact;261:56-62, 2017 Jan 05.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:This work aimed to determine the chemical fingerprint of hydroethanolic extract of leaves of Caryocar coriaceum (HELCC) and the gastroprotective activity. The chemical fingerprint of HELCC was analyzed by HPLC-DAD, to quantify total phenols and flavonoids were carried out by Folin-Ciocalteu reagent and aluminum chloride assay, while in vitro antioxidant activity was evaluated by the DPPH method. The methods used to determine pharmacological activity were: gastroprotective screening test in classical models of induced acute and chronic gastric lesions and physical barrier test. Further assays were performed to demonstrate the involvement of NO, prostaglandins, ATP-dependent potassium channels, TRPV, noradrenergic α2 receptors, histamines, and opioids. The DPPH method demonstrated the antioxidant activity of the extract, in vitro, explained by the presence of polyphenols and flavonoids. Oral administration of the extract, previously dissolved in deionized water, at a dose of 100 mg/kg decreased the lesions induced by indomethacin, acidified ethanol, ethanol and acetic acid by 75.0, 72.8, 69.4 and 86.2% respectively. It was demonstrated that opioid receptors, α -adrenergic receptors and primary afferent neurons sensitive to capsaicin were involved in the mechanism of gastric protection, in addition to the contribution of NO and prostaglandins. The results show that extract is a promising candidate for the treatment of gastric ulcers.
[Mh] Termos MeSH primário: Ericales/química
Etanol/química
Extratos Vegetais/uso terapêutico
Folhas de Planta/química
Substâncias Protetoras/uso terapêutico
Úlcera Gástrica/tratamento farmacológico
Água/química
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Capsaicina/análogos & derivados
Capsaicina/farmacologia
Capsaicina/uso terapêutico
Cromatografia Líquida de Alta Pressão
Doença Crônica
Modelos Animais de Doenças
Feminino
Flavonoides/análise
Motilidade Gastrointestinal
Glibureto/farmacologia
Glibureto/uso terapêutico
Histamina/farmacologia
Histamina/uso terapêutico
Indometacina
Masculino
Camundongos
Muco/efeitos dos fármacos
NG-Nitroarginina Metil Éster/farmacologia
NG-Nitroarginina Metil Éster/uso terapêutico
Naloxona/farmacologia
Naloxona/uso terapêutico
Fenóis/análise
Fitoterapia
Extratos Vegetais/farmacologia
Úlcera Gástrica/patologia
Ioimbina/farmacologia
Ioimbina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Flavonoids); 0 (Phenols); 0 (Plant Extracts); 0 (Protective Agents); 059QF0KO0R (Water); 2Y49VWD90Q (Yohimbine); 36B82AMQ7N (Naloxone); 3K9958V90M (Ethanol); 820484N8I3 (Histamine); LFW48MY844 (capsazepine); S07O44R1ZM (Capsaicin); SX6K58TVWC (Glyburide); V55S2QJN2X (NG-Nitroarginine Methyl Ester); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE


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[PMID]:27739080
[Au] Autor:Xiang X; Shang B; Wang X; Chen Q
[Ad] Endereço:Affiliated Dongfeng Hospital, Hubei University of Medicine, Hubei, China.
[Ti] Título:PEEK tube-based online solid-phase microextraction-high-performance liquid chromatography for the determination of yohimbine in rat plasma and its application in pharmacokinetics study.
[So] Source:Biomed Chromatogr;31(4), 2017 Apr.
[Is] ISSN:1099-0801
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Yohimbine is a novel compound for the treatment of erectile dysfunction derived from natural products, and pharmacokinetic study is important for its further development as a new medicine. In this work, we developed a novel PEEK tube-based solid-phase microextraction (SPME)-HPLC method for analysis of yohimbine in plasma and further for pharmacokinetic study. Poly (AA-EGDMA) was synthesized inside a PEEK tube as the sorbent for microextraction of yohimbine, and parameters that could influence extraction efficiency were systematically investigated. Under optimum conditions, the PEEK tube-based SPME method exhibits excellent enrichment efficiency towards yohimbine. By using berberine as internal standard, an online SPME-HPLC method was developed for analysis of yohimbine in human plasma sample. The method has wide linear range (2-1000 ng/mL) with an R of 0.9962; the limit of detection was determined and was as low as 0.1 ng/mL using UV detection. Finally, a pharmacokinetic study of yohimbine was carried out by the online SPME-HPLC method and the results have been compared with those of reported methods.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Microextração em Fase Sólida/métodos
Ioimbina/sangue
Ioimbina/farmacocinética
[Mh] Termos MeSH secundário: Administração Oral
Animais
Berberina/sangue
Cromatografia Líquida de Alta Pressão/normas
Estabilidade de Medicamentos
Desenho de Equipamento
Limite de Detecção
Masculino
Ratos Sprague-Dawley
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Microextração em Fase Sólida/instrumentação
Ioimbina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0I8Y3P32UF (Berberine); 2Y49VWD90Q (Yohimbine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170317
[Lr] Data última revisão:
170317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161015
[St] Status:MEDLINE
[do] DOI:10.1002/bmc.3866


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[PMID]:27028940
[Au] Autor:Neha; Ansari MM; Khan HA
[Ad] Endereço:Heavy Metal and Clinical Toxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard, Hamdard Nagar, New Delhi, 110062, India.
[Ti] Título:Yohimbine hydrochloride ameliorates collagen type-II-induced arthritis targeting oxidative stress and inflammatory cytokines in Wistar rats.
[So] Source:Environ Toxicol;32(2):619-629, 2017 Feb.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis (RA) is the most common type of chronic inflammatory disease which is triggered by dysfunction in the immune system which in turn affects synovial joints. Current treatment of RA with NSAIDs and DMRDs is limited by their side effect. As a result, the interest in alternative, well tolerated anti-inflammatory remedies has re-emerged. Our aim was to evaluate the antioxidant and anti-inflammatory activities underlying the anti-RA effect of Yohimbine hydrochloride (YCL) in collagen induced arthritis (CIA) in Wistar rats. The YCL was administered at doses of 5 and 10 mg kg body weight once daily for 28 days. The effects of treatment in the rats were assessed by biochemical parameter (articular elastase, LPO, GSH, catalase, SOD), hematological parameter (ESR, WBC, C-reactive protein (CRP), immunohistochemical expression (COX2, TNF-α, and NF-κB), and histological changes in joints. YCL showed anti-RA efficacy as it significantly reduced articular elastase, LPO and catalase level and ameliorates histological changes. This is in addition to its antioxidant efficacy as YCL shown a significant increase in GSH and SOD level. Also, YCL showed effective anti-inflammatory activity as it significantly decreased the expression of COX-2, TNF-α, and NF-ĸB. The therapeutic effect of YCL against RA was also evident from lower arthritis scoring and reduced hematological parameter (ESR, WBC, and C-reactive protein level). The abilities to inhibit proinflammatory cytokines and modulation of antioxidant states that the protective effect of YCL on arthritis rats might be mediated via the modulation of the immune system. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 619-629, 2017.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Antioxidantes/farmacologia
Artrite Experimental/tratamento farmacológico
Artrite Reumatoide/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Ioimbina/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/uso terapêutico
Antioxidantes/uso terapêutico
Artrite Experimental/imunologia
Artrite Experimental/metabolismo
Artrite Reumatoide/metabolismo
Cartilagem Articular/efeitos dos fármacos
Cartilagem Articular/patologia
Catalase/metabolismo
Colágeno Tipo II
Ciclo-Oxigenase 2/metabolismo
Avaliação Pré-Clínica de Medicamentos
Feminino
Glutationa/metabolismo
Peroxidação de Lipídeos
NF-kappa B/metabolismo
Ratos
Ratos Wistar
Fator de Necrose Tumoral alfa/metabolismo
Ioimbina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Collagen Type II); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); 2Y49VWD90Q (Yohimbine); EC 1.11.1.6 (Catalase); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22264


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[PMID]:27793651
[Au] Autor:Fotso Soh J; Strong HR; Daneshtalab N; Tabrizchi R
[Ad] Endereço:Division of BioMedical Sciences, Faculty of Medicine Memorial University, St. John's, NL, Canada.
[Ti] Título:The effect of inflammation on sympathetic nerve mediated contractions in rat isolated caudal artery.
[So] Source:Eur J Pharmacol;792:54-62, 2016 Dec 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic inflammatory process(es) contributes to changes in vascular function in a variety of diseases. Sympathetic nerve-mediated responses in blood vessels play a pivotal role in regular physiological functions. We tested the hypothesis that sympathetic neuro-effector function will be altered as consequence of inflammatory state. Sympathetic nerve-mediated contractions and alpha adrenergic receptor expressions were evaluated in isolated caudal arteries of rats treated with saline and Complete Freund's adjuvant (CFA). While CFA-treated animals had significantly higher plasma levels of tumor necrosis factor-alpha compared to saline, blood pressure remained unchanged. Immunofluorescence revealed increased expression of ionized calcium adapter binding molecule-1 in the adventitia of blood vessels from CFA-treated animals compared to saline. In isolated arteries, electrical field stimulations between 1.25 and 40Hz resulted in frequency-dependent contractions that wasabolished by tetrodotoxin. Neurogenic contractions from CFA groups were significantly greater than saline. While the presence of alpha -adrenoceptor antagonist (prazosin) significantly inhibited contractions at lower frequencies of stimulation (1.25-5Hz) in isolated arteries of CFA-treated rats compared to controls, alpha -adrenoceptor antagonist (rauwolscine) had modest effects. Inhibition of neuronal reuptake by cocaine comparably enhanced field-stimulated responses in vessels of experimental and control animals. Immunofluorescence revealed a difference in expression of alpha - and alpha -adrenoceptors in the endothelium of blood vessels of CFA compared to saline controls. Collectively, our observations lend support to enhanced neurogenic contractions in blood vessels of inflamed animals possibly attributing to alterations in responsiveness and/or distribution of post-junctional alpha -adrenoceptors.
[Mh] Termos MeSH primário: Aorta/fisiopatologia
Sistema Nervoso Simpático/fisiopatologia
Vasoconstrição
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Proteínas de Ligação ao Cálcio/metabolismo
Cocaína/farmacologia
Dioxanos/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Inflamação/metabolismo
Inflamação/fisiopatologia
Masculino
Proteínas dos Microfilamentos/metabolismo
Prazosina/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores Adrenérgicos alfa 1/metabolismo
Receptores Adrenérgicos alfa 2/metabolismo
Sistema Nervoso Simpático/efeitos dos fármacos
Fator de Necrose Tumoral alfa/sangue
Vasoconstrição/efeitos dos fármacos
Ioimbina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Dioxanes); 0 (Microfilament Proteins); 0 (Receptors, Adrenergic, alpha-1); 0 (Receptors, Adrenergic, alpha-2); 0 (Tumor Necrosis Factor-alpha); 2Y49VWD90Q (Yohimbine); E9H51OIT2B ((2-(2',6'-dimethoxy)phenoxyethylamino)methylbenzo-1,4-dioxane); I5Y540LHVR (Cocaine); XM03YJ541D (Prazosin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  10 / 5441 MEDLINE  
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Fotocópia
[PMID]:27706026
[Au] Autor:Ok SH; Kwon SC; Baik J; Hong JM; Oh J; Han JY; Sohn JT
[Ad] Endereço:Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, Jinju-si 52727, Korea. mdoksh@naver.com.
[Ti] Título:Dexmedetomidine-Induced Contraction Involves CPI-17 Phosphorylation in Isolated Rat Aortas.
[So] Source:Int J Mol Sci;17(10), 2016 Sep 30.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Dexmedetomidine, a highly selective α-2 adrenoceptor agonist, produces vasoconstriction, which leads to transiently increased blood pressure. The goal of this study was to investigate specific protein kinases and the associated cellular signal pathways responsible for the increased calcium sensitization induced by dexmedetomidine in isolated rat aortas, with a particular focus on phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17). The effect of Y-27632 and chelerythrine on the dexmedetomidine-induced intracellular calcium concentration ([Ca ] ) and tension were assessed using fura-2-loaded aortic strips. The effects of rauwolscine, Y-27632, chelerythrine, and ML-7 hydrochloride on the dexmedetomidine-induced phosphorylation of CPI-17 or of the 20-kDa regulatory light chain of myosin (MLC ) were investigated in rat aortic vascular smooth muscle cells. The effects of rauwolscine, Y-27632, and chelerythrine on the membrane translocation of Rho-kinase and protein kinase C (PKC) phosphorylation induced by dexmedetomidine were assessed. Y-27632 and chelerythrine each reduced the slopes of the [Ca ] -tension curves of dexmedetomidine-induced contraction, and Y-27632 more strongly reduced these slopes than did chelerythrine. Rauwolscine, Y-27632, chelerythrine, and ML-7 hydrochloride attenuated the dexmedetomidine-induced phosphorylation of CPI-17 and MLC . Taken together, these results suggest that dexmedetomidine-induced contraction involves calcium sensitization, which appears to be mediated by CPI-17 phosphorylation via Rho-kinase or PKC.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Aorta/efeitos dos fármacos
Dexmedetomidina/farmacologia
Contração Muscular/efeitos dos fármacos
Proteínas Musculares/metabolismo
Fosfoproteínas/metabolismo
[Mh] Termos MeSH secundário: Amidas/farmacologia
Animais
Aorta/citologia
Aorta/metabolismo
Benzofenantridinas/farmacologia
Cálcio/metabolismo
Células Cultivadas
Fura-2/química
Técnicas In Vitro
Masculino
Músculo Liso Vascular/citologia
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Cadeias Leves de Miosina/metabolismo
Fosforilação/efeitos dos fármacos
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/metabolismo
Piridinas/farmacologia
Ratos
Ratos Sprague-Dawley
Ioimbina/farmacologia
Quinases Associadas a rho/antagonistas & inibidores
Quinases Associadas a rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Amides); 0 (Benzophenanthridines); 0 (Muscle Proteins); 0 (Myosin Light Chains); 0 (Phosphoproteins); 0 (Ppp1r14a protein, rat); 0 (Pyridines); 138381-45-0 (Y 27632); 2Y49VWD90Q (Yohimbine); 67VB76HONO (Dexmedetomidine); E3B045W6X0 (chelerythrine); EC 2.7.11.1 (rho-Associated Kinases); EC 2.7.11.13 (Protein Kinase C); SY7Q814VUP (Calcium); TSN3DL106G (Fura-2)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE



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