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[PMID]:29236753
[Au] Autor:Meyer MJ; Seitz T; Brockmöller J; Tzvetkov MV
[Ad] Endereço:Institute of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany.
[Ti] Título:Effects of genetic polymorphisms on the OCT1 and OCT2-mediated uptake of ranitidine.
[So] Source:PLoS One;12(12):e0189521, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ranitidine (Zantac®) is a H2-receptor antagonist commonly used for the treatment of acid-related gastrointestinal diseases. Ranitidine was reported to be a substrate of the organic cation transporters OCT1 and OCT2. The hepatic transporter OCT1 is highly genetically variable. Twelve major alleles confer partial or complete loss of OCT1 activity. The effects of these polymorphisms are highly substrate-specific and therefore difficult to predict. The renal transporter OCT2 has a common polymorphism, Ala270Ser, which was reported to affect OCT2 activity. AIM: In this study we analyzed the effects of genetic polymorphisms in OCT1 and OCT2 on the uptake of ranitidine and on its potency to inhibit uptake of other drugs. METHODS AND RESULTS: We characterized ranitidine uptake using HEK293 and CHO cells stably transfected to overexpress wild type OCT1, OCT2, or their naturally occurring allelic variants. Ranitidine was transported by wild-type OCT1 with a Km of 62.9 µM and a vmax of 1125 pmol/min/mg protein. Alleles OCT1*5, *6, *12, and *13 completely lacked ranitidine uptake. Alleles OCT1*2, *3, *4, and *10 had vmax values decreased by more than 50%. In contrast, OCT1*8 showed an increase of vmax by 25%. The effects of OCT1 alleles on ranitidine uptake strongly correlated with the effects on morphine uptake suggesting common interaction mechanisms of both drugs with OCT1. Ranitidine inhibited the OCT1-mediated uptake of metformin and morphine at clinically relevant concentrations. The inhibitory potency for morphine uptake was affected by the OCT1*2 allele. OCT2 showed only a limited uptake of ranitidine that was not significantly affected by the Ala270Ser polymorphism. CONCLUSIONS: We confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine's potential to cause drug-drug interactions. The effects of the frequent OCT1 polymorphisms on ranitidine pharmacokinetics in humans remain to be analyzed.
[Mh] Termos MeSH primário: Antagonistas dos Receptores Histamínicos H2/farmacocinética
Transportador 1 de Cátions Orgânicos/metabolismo
Transportador 2 de Cátion Orgânico/metabolismo
Polimorfismo Genético
Ranitidina/farmacocinética
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetulus
Células HEK293
Seres Humanos
Transportador 1 de Cátions Orgânicos/genética
Transportador 2 de Cátion Orgânico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H2 Antagonists); 0 (Organic Cation Transporter 1); 0 (Organic Cation Transporter 2); 884KT10YB7 (Ranitidine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189521


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[PMID]:28842999
[Au] Autor:Carroll TL; Werner A; Nahikian K; Dezube A; Roth DF
[Ad] Endereço:Department of Surgery, Division of Otolaryngology, Brigham and Women's Hospital, Boston, Massachusetts, U.S.A.
[Ti] Título:Rethinking the laryngopharyngeal reflux treatment algorithm: Evaluating an alternate empiric dosing regimen and considering up-front, pH-impedance, and manometry testing to minimize cost in treating suspect laryngopharyngeal reflux disease.
[So] Source:Laryngoscope;127 Suppl 6:S1-S13, 2017 Oct.
[Is] ISSN:1531-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES/HYPOTHESIS: Empiric proton pump inhibitor (PPI) trials for laryngopharyngeal reflux (LPR) are common. A majority of the patients respond to acid suppression. This work intends to evaluate once-daily, 40 mg omeprazole and once-nightly, 300 mg ranitidine (QD/QHS) dosing as an alternative regimen, and use this study's cohort to evaluate empiric regimens prescribed for LPR as compared to up-front testing with pH impedance multichannel intraluminal impedance (MII) with dual pH probes and high-resolution manometry (HRM) for potential cost minimization. STUDY DESIGN: Retrospective cohort review and cost minimization study. METHODS: A chart review identified patients diagnosed with LPR. All subjects were treated sequentially and outcomes recorded. Initial QD/QHS dosing increased after 3 months to BID if no improvement and ultimately prescribed MII and HRM if they failed BID dosing. Decision tree diagrams were constructed to determine costs of two empiric regimens and up-front MII and HRM. RESULTS: Ninety-seven subjects met the criteria. Responders and nonresponders to empiric therapy were identified. Seventy-two subjects (74%) responded. Forty-eight (67% of responders and 49% of all) improved with QD/QHS dosing. Forty-nine (51%) subjects escalated to BID dosing. Twenty-four subjects (33% of responders and 25% of all) improved on BID therapy. Twenty-five subjects (26%) did not respond to acid suppression. Average weighted cost was $1,897.00 per patient for up-front testing, $3,033.00 for initial BID, and $3,366.00 for initial QD/QHS. CONCLUSIONS: An alternate QD/QHS regimen improved the majority who presented with presumed LPR. Cost estimates demonstrate that the QD/QHS regimen was more expensive than the initial BID high-dose PPI for 6 months. Overall per-patient cost appears less with up-front MII and HRM. LEVEL OF EVIDENCE: 4. Laryngoscope, 127:S1-S13, 2017.
[Mh] Termos MeSH primário: Algoritmos
Antiulcerosos/administração & dosagem
Análise Custo-Benefício
Monitoramento do pH Esofágico/economia
Refluxo Laringofaríngeo/tratamento farmacológico
Manometria/economia
Inibidores da Bomba de Prótons/administração & dosagem
[Mh] Termos MeSH secundário: Antiulcerosos/economia
Esquema de Medicação
Quimioterapia Combinada/economia
Quimioterapia Combinada/métodos
Impedância Elétrica
Monitoramento do pH Esofágico/métodos
Feminino
Seres Humanos
Refluxo Laringofaríngeo/economia
Refluxo Laringofaríngeo/fisiopatologia
Masculino
Manometria/métodos
Meia-Idade
Omeprazol/administração & dosagem
Omeprazol/economia
Inibidores da Bomba de Prótons/economia
Ranitidina/administração & dosagem
Ranitidina/economia
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Ulcer Agents); 0 (Proton Pump Inhibitors); 884KT10YB7 (Ranitidine); KG60484QX9 (Omeprazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE
[do] DOI:10.1002/lary.26806


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[PMID]:28774600
[Au] Autor:Lv J; Wang L; Li Y
[Ad] Endereço:School of Environment and Architecture, University of Shanghai for Science and Technology, Shanghai 200093, China; State Key Laboratory of Pollution Control and Resource Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai 200092, China. Electronic address: lujuan@usst.edu.cn.
[Ti] Título:Characterization of N-nitrosodimethylamine formation from the ozonation of ranitidine.
[So] Source:J Environ Sci (China);58:116-126, 2017 Aug.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:N-nitrosodimethylamine (NDMA) is an emerging disinfection by-product which is formed during water disinfection in the presence of amine-based precursors. Ranitidine, as one kind of amine-based pharmaceuticals, has been identified as NDMA precursor with high NDMA molar conversion during chloramination. This study focused on the characterization of NDMA formation during ozonation of ranitidine. Influences of operational variables (ozone dose, pH value) and water matrix on NDMA generation as well as ranitidine degradation were evaluated. The results indicate high reactivity of ranitidine with ozone. Dimethylamine (DMA) and NDMA were generated due to ranitidine oxidation. High pH value caused more NDMA accumulation. NDMA formation was inhibited under acid conditions (pH≤5) mainly due to the protonation of amines. Water matrix such as HCO and humic acid impacted NDMA generation due to OH scavenging. Compared with OH, ozone molecules dominated the productions of DMA and NDMA. However, OH was a critical factor in NDMA degradation. Transformation products of ranitidine during ozonation were identified using gas chromatography-mass spectrometry. Among these products, just DMA and N,N-dimethylformamide could contribute to NDMA formation due to the DMA group in the molecular structures. The NDMA formation pathway from ranitidine ozonation was also proposed.
[Mh] Termos MeSH primário: Dimetilnitrosamina/química
Modelos Químicos
Ozônio/química
Ranitidina/química
Poluentes Químicos da Água/química
[Mh] Termos MeSH secundário: Dimetilaminas
Dimetilnitrosamina/análise
Desinfecção
Oxirredução
Poluentes Químicos da Água/análise
Purificação da Água/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dimethylamines); 0 (Water Pollutants, Chemical); 66H7ZZK23N (Ozone); 884KT10YB7 (Ranitidine); ARQ8157E0Q (dimethylamine); M43H21IO8R (Dimethylnitrosamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


  4 / 5055 MEDLINE  
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Cipolotti, Rosana
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[PMID]:28558748
[Au] Autor:Santana RNS; Santos VS; Ribeiro-Júnior RF; Freire MS; Menezes MAS; Cipolotti R; Gurgel RQ
[Ad] Endereço:Department of Medicine, Federal University of Sergipe, R. Cláudio Batista, s/n - Cidade Nova, Aracaju, 49060-108, Brazil.
[Ti] Título:Use of ranitidine is associated with infections in newborns hospitalized in a neonatal intensive care unit: a cohort study.
[So] Source:BMC Infect Dis;17(1):375, 2017 May 30.
[Is] ISSN:1471-2334
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The inhibition of gastric acid secretion with ranitidine is frequently prescribed off-label to newborns admitted to neonatal intensive care units (NICU). Some studies show that the use of inhibitors of gastric acid secretion (IGAS) may predispose to infections and necrotising enterocolitis (NEC), but there are few data to confirm this association. This study aimed to compare the rates of neonatal infections and NEC among preterm infants (<37 weeks gestation) hospitalised in a NICU exposed or not to treatment with ranitidine. METHODS: A retrospective cohort study was conducted with all consecutive preterm newborns admitted to a NICU between August-2014 and October-2015. The rates of infection, NEC, and death of newborns exposed or not to ranitidine were recorded. RESULTS: A total of 300 newborns were enrolled, of which 115 had received ranitidine and 185 had not. The two groups were similar with regard to the main demographic and clinical characteristics. Forty-eight (41.7%) of the 115 infants exposed to ranitidine and 49 (26.5%) of the 185 infants not exposed were infected (RR = 1.6, 95%CI 1.1-2.2, p = 0.006). The late onset (>48 h) blood culture positive infection rate was higher in the group exposed to ranitidine than in the untreated group (13.0% vs. 3.8%, p = 0.001). There was no significant association between the use of ranitidine and NEC (Bell stage >II) (p = 0.36). The mortality rate risk was 4-fold higher in infants receiving ranitidine (16.5% vs. 8.6%, p < 0.001). CONCLUSION: Ranitidine use in neonates was associated with an increased risk of infections and mortality, but not with NEC.
[Mh] Termos MeSH primário: Infecção Hospitalar/epidemiologia
Enterocolite Necrosante/epidemiologia
Ranitidina/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Brasil/epidemiologia
Estudos de Coortes
Infecção Hospitalar/induzido quimicamente
Infecção Hospitalar/etiologia
Enterocolite Necrosante/induzido quimicamente
Enterocolite Necrosante/etiologia
Feminino
Idade Gestacional
Mortalidade Hospitalar
Seres Humanos
Lactente
Recém-Nascido
Recém-Nascido Prematuro
Unidades de Terapia Intensiva Neonatal/estatística & dados numéricos
Masculino
Ranitidina/administração & dosagem
Ranitidina/uso terapêutico
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
884KT10YB7 (Ranitidine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1186/s12879-017-2482-x


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[PMID]:28529239
[Au] Autor:Zhang X; Zhang Y; Han H; Yang J; Xu B; Wang B; Zhang T
[Ad] Endereço:Experiment Center for Teaching and Learning, Shanghai University of Traditional Chinese Medicine.
[Ti] Título:Formulation Optimization of Gastro-Retention Tablets of Paeonol and Efficacy in Treatment of Experimental Gastric Ulcer.
[So] Source:Chem Pharm Bull (Tokyo);65(8):706-713, 2017 Aug 01.
[Is] ISSN:1347-5223
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:This study aims to develop a gastroretentive sustained-release drug delivery system of paeonol using floating properties and to investigate its therapeutic effects in rat models. The gastric retention tablets of paeonol (GRT-Ps) were prepared by a direct compression method, and the Box-Behnken design was used to optimize its formulation. The optimized formulation containing 15% NaHCO and a 2 : 1 ratio of paeonol and HPMC-K4M floated within 1 min and remained afloat for more than 8 h in the simulated gastric fluid (200 mL, pH=1.2) and simultaneously showed the desired sustained drug release. Moreover, small tablets (3 mm) were prepared according to the same formulation and the process technology of big tablets (8 mm). A similar drug release behavior was observed between two kinds of tablets (f =52), and then the evaluations of efficacy and retention capacity in vivo were conducted with small tablets. In vivo retention studies showed that the T (2 h) of GRT-P in rat stomachs was significantly extended compared with the T (0.5 h) of normal reference preparation. Compared with the model group, low and high doses of GRT-P could significantly inhibit the increase of malondialdehyde (MDA) in serum. Studies showed that the higher MDA content in inflammation tissue increases the inflammatory response. The ulcer inhibition rates of GRT-P in the high-dose group were 59.0 and 64.1% in the ranitidine group. Results indicated that GRT-Ps had the potential for a sustained drug release and an enhanced gastric residence time with relatively high drug concentrations in the tissue distribution.
[Mh] Termos MeSH primário: Acetofenonas/uso terapêutico
Composição de Medicamentos
Úlcera Gástrica/tratamento farmacológico
[Mh] Termos MeSH secundário: Acetofenonas/administração & dosagem
Acetofenonas/química
Administração Oral
Animais
Modelos Animais de Doenças
Sistemas de Liberação de Medicamentos
Desenho de Drogas
Masculino
Ranitidina
Ratos
Ratos Sprague-Dawley
Úlcera Gástrica/induzido quimicamente
Comprimidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Tablets); 3R834EPI82 (paeonol); 884KT10YB7 (Ranitidine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE
[do] DOI:10.1248/cpb.c16-00993


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[PMID]:28512370
[Au] Autor:Herrera-Mozo I; Sanz-Gallen P; Martí-Amengual G
[Ad] Endereço:Clinica Creu Blanca, Barcelona, Spain (Unit of Allergy). herreramozo.i@gmail.com.
[Ti] Título:Occupational contact allergy to omeprazole and ranitidine.
[Ti] Título:Occupational contact allergy to omeprazole and ranitidine..
[So] Source:Med Pr;68(3):433-435, 2017 May 16.
[Is] ISSN:0465-5893
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Omeprazole is a proton pump inhibition and ranitidine is an H2 histamine receptor antagonist widely used in the treatment of gastroesophageal reflex disease, peptic ulcer disease, Zollinger-Ellison syndrome and as a protector of the gastric mucosae. We report a case of occupational contact allergy to omeprazole and ranitidine. A 48-year-old man, with no pre-existing history of atopy or lifestyle factors. He neither had any medical history of consumption of drugs such as ranitidine and omeprazole. He worked for 19 months in the pharmaceutical company that manufactured ranitidine base. He presented rash in the face and eczema on the dorsum of the hands with itching. The study by prick tests with ranitidine gave negative response. Patch testing with ranitidine base and ranitidine hydrochloride gave positive response. A month later, when the patient was asymptomatic he returned to the pharmaceutical company, being switched from this previous job to the reactor manufacturing omeprazole. A few days after that, he presented erythematous eruptions involving face and neck with itching. Prick tests, path tests and in vitro laboratories studies with omeprazole gave positives. In this case the patient presented hypersensitivity type I at omeprazole and hypersensitivity type IV at omeprazole and ranitidine. Our aportation indicates the importance of careful analysis of the occupational exposure histories of patients with the suspected type I or type IV hypersensitivity to allergens, to determine whether work exposure is the cause. Med Pr 2017;68(3):433-435.
[Mh] Termos MeSH primário: Dermatite Ocupacional/diagnóstico por imagem
Antagonistas dos Receptores Histamínicos H2/efeitos adversos
Omeprazol/efeitos adversos
Inibidores da Bomba de Prótons/efeitos adversos
Ranitidina/efeitos adversos
[Mh] Termos MeSH secundário: Eczema/induzido quimicamente
Exantema/induzido quimicamente
Seres Humanos
Masculino
Meia-Idade
Testes do Emplastro
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H2 Antagonists); 0 (Proton Pump Inhibitors); 884KT10YB7 (Ranitidine); KG60484QX9 (Omeprazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE


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[PMID]:28400101
[Au] Autor:Singh DP; Borse SP; Nivsarkar M
[Ad] Endereço:Department of Pharmacology and Toxicology, B. V. Patel Pharmaceutical Education and Research Development (PERD) Centre, Thaltej, Ahmedabad, Gujarat, 380054, India; Registered Ph.D Scholar (External) at Institute of Pharmacy, NIRMA University, Sarkhej-Gandhinagar Highway, Ahmedabad, Gujarat 382481, India.
[Ti] Título:Overcoming the exacerbating effects of ranitidine on NSAID-induced small intestinal toxicity with quercetin: Providing a complete GI solution.
[So] Source:Chem Biol Interact;272:53-64, 2017 Jun 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:There is a need to find/discover novel leads to treat complex and/or multi-factorial-pathogenic disease(s) like Nonsteroidal anti-inflammatory drugs (NSAID)-induced gastroenteropathy or gastrointestinal (GI) toxicity as it has emerged as an important medical and socioeconomic problem. There is no approved therapeutic strategy to prevent NSAID-induced enteropathic damage and highly effective gastro-protective drugs such as ranitidine hydrochloride (RAN) exacerbate it. In this purview, the multi target drug discovery approach (MTDD), combination approach and hit to lead strategies based on the foundation of ethnopharmacology and/or reverse pharmacology holds strong potential. Hence, the primary objectives of the current study were to explore the mechanism behind the preventative/curative effects of quercetin (QCT) on RAN exacerbated diclofenac sodium (DIC)-induced enteropathic damage and to assess the effects of co-administration of QCT and RAN on DIC-induced gastropathic damage in rats. Rats were treated twice daily with QCT (35, 50 and 100 mg kg PO) and/or RAN (15 mg kg PO) or vehicle for a total of 10 days. In some experiments, DIC (9 mg kg ) was administered orally twice daily for the final 5 days of RAN/QCT + RAN/vehicle administration. Rats in all the groups were fasted after the last dose on 9th day (free access to water). 12 h after the last dose on 10th day, rats were euthanized and their GI tracts were assessed for haemorrhagic damage, alteration in xanthine oxidase (XO) activity, lipid peroxidation, intestinal permeability and GI luminal pH alterations along with haematological and biochemical estimations. The macroscopic, haematological, biochemical and histological evidences suggested that, though, RAN prevented the DIC-induced gastric injury, it exacerbated enteropathic damage. However, QCT not only significantly attenuated the RAN-induced exacerbation of enteropathic damage caused by DIC at the doses of 50 and 100 mg kg , but, this combination provided complete GI safety against the toxic effects of DIC too. The mechanisms behind the gastro-enteroprotective ability of QCT may be related to its ability to inhibit XO activity thus, preventing enhanced oxidative stress on GI tissues, prevent lipid peroxidation, IP alteration and alteration in GI luminal pH. The preventative effects of QCT on NSAID-induced gastroenteropathy were ably supported by the QCT induced prevention of GI blood loss and serum protein loss. These pharmaco-mechanistic results of QCT are aligning to combination based MTDD approach and hence we propose it as a promising lead to treat NSAID-gastroenteropahty and related complications.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/toxicidade
Intestino Delgado/efeitos dos fármacos
Quercetina/toxicidade
Ranitidina/farmacologia
Estômago/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Diclofenaco/toxicidade
Ingestão de Alimentos/efeitos dos fármacos
Gastroenteropatias/induzido quimicamente
Gastroenteropatias/patologia
Gastroenteropatias/prevenção & controle
Intestino Delgado/metabolismo
Intestino Delgado/patologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Malondialdeído/análise
Estresse Oxidativo/efeitos dos fármacos
Permeabilidade/efeitos dos fármacos
Ranitidina/uso terapêutico
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
Estômago/metabolismo
Estômago/patologia
Xantina Oxidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Reactive Oxygen Species); 144O8QL0L1 (Diclofenac); 4Y8F71G49Q (Malondialdehyde); 884KT10YB7 (Ranitidine); 9IKM0I5T1E (Quercetin); EC 1.17.3.2 (Xanthine Oxidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE


  8 / 5055 MEDLINE  
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[PMID]:28177773
[Au] Autor:Oliveira de Lima VC; de Araújo Machado RJ; Vieira Monteiro NK; de Lyra IL; da Silva Camillo C; Coelho Serquiz A; Silva de Oliveira A; da Silva Rufino FP; Leal Lima Maciel B; Ferreira Uchôa A; Antunes Dos Santos E; de Araújo Morais AH
[Ad] Endereço:a Biochemistry Department, Biosciences Center, Federal University of Rio Grande do Norte, 59078-970 Natal, RN, Brazil.
[Ti] Título:Gastroprotective and antielastase effects of protein inhibitors from Erythrina velutina seeds in an experimental ulcer model.
[So] Source:Biochem Cell Biol;95(2):243-250, 2017 Apr.
[Is] ISSN:1208-6002
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Trypsin and chymotrypsin inhibitors from Erythrina velutina seeds have been previously isolated by our group. In previous studies using a sepsis model, we demonstrated the antitumor and anti-inflammatory action of these compounds. This study aimed to evaluate the gastroprotective and antielastase effects of protein inhibitors from E. velutina seeds in an experimental stress-induced ulcer model. Two protein isolates from E. velutina seeds, with antitrypsin (PIAT) and antichymotrypsin (PIAQ) activities, were tested. Both protein isolates showed a high affinity and inhibitory effect against human neutrophil elastase, with 84% and 85% inhibition, respectively. Gastric ulcer was induced using ethanol (99%) in 6 groups of animals (female Wistar rats, n = 6). Before ulcer induction, these animals were treated for 5 days with one of the following: (1) PIAT (0.2 mg·kg ), (2) PIAT (0.4 mg·kg ), (3) PIAQ (0.035 mg·kg ), (4) ranitidine hydrochloride (50 mg·kg ), (5) saline solution (0.9%), or (6) no intervention (sham). Both PIAT and PIAQ protected gastric mucosa, preventing hemorrhagic lesions, edema, and mucus loss. No histologic toxic effects of PIAT or PIAQ were seen in liver and pancreatic cells. Our results show that protein isolates from E. velutina seeds have potential gastroprotective effects, placing these compounds as natural candidates for gastric ulcer prevention.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Inibidores Enzimáticos/farmacologia
Erythrina/química
Fármacos Gastrointestinais/farmacologia
Fitoterapia
Úlcera Gástrica/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/isolamento & purificação
Modelos Animais de Doenças
Inibidores Enzimáticos/isolamento & purificação
Etanol
Feminino
Mucosa Gástrica/efeitos dos fármacos
Mucosa Gástrica/enzimologia
Mucosa Gástrica/patologia
Fármacos Gastrointestinais/isolamento & purificação
Seres Humanos
Elastase de Leucócito/antagonistas & inibidores
Elastase de Leucócito/metabolismo
Extratos Vegetais/química
Ranitidina/farmacologia
Ratos
Ratos Wistar
Sementes/química
Úlcera Gástrica/induzido quimicamente
Úlcera Gástrica/enzimologia
Úlcera Gástrica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Enzyme Inhibitors); 0 (Gastrointestinal Agents); 0 (Plant Extracts); 3K9958V90M (Ethanol); 884KT10YB7 (Ranitidine); EC 3.4.21.37 (Leukocyte Elastase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170525
[Lr] Data última revisão:
170525
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1139/bcb-2016-0034


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[PMID]:28092180
[Au] Autor:Soliman NA; Zineldeen DH; Katary MA; Ali DA
[Ad] Endereço:a Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt.
[Ti] Título:N-acetylcysteine a possible protector against indomethacin-induced peptic ulcer: crosstalk between antioxidant, anti-inflammatory, and antiapoptotic mechanisms.
[So] Source:Can J Physiol Pharmacol;95(4):396-403, 2017 Apr.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:This study investigated the gastroprotective effects of N-acetylcysteine (NAC) against indomethacin-induced gastric ulcer in rats. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg). 50 male albino rats were allocated into 5 equal groups: control group received normal saline orally, indomethacin group rats received normal saline orally for 5 days and indomethacin (50 mg/kg) on the last day, ranitidine group received ranitidine (reference drug) orally for 5 days (50 mg/kg) before receiving indomethacin (50 mg/kg) on the last day, and NAC groups received NAC orally at 300 and 500 mg/kg, respectively, for 5 days before receiving indomethacin (50 mg/kg) on the last day. Gastric tissue interleukin-1ß (IL-1ß), interferon-γ (IFN-γ), and caspase-3 levels were immunoassayed. Total thiol (T-SH), myeloperoxidase (MPO), and glucose-6-phosphate dehydrogenase (G6PD) were determined by spectrophotometry. Cytokine-induced neutrophil chemoattractant 2α (CINC-2α) gene expression was evaluated in addition to Bcl-2 immunohistochemistry. Pretreatment with NAC improved the inflammatory, apoptotic, and redox status in a dose-dependent manner particularly in NAC 500 mg/kg pretreated group. These results show a role for NAC in improving indomethacin-induced gastric ulceration via antioxidative, antiapoptotic, and anti-inflammatory interactive mechanisms.
[Mh] Termos MeSH primário: Acetilcisteína/uso terapêutico
Antioxidantes/uso terapêutico
Apoptose/efeitos dos fármacos
Oxirredução/efeitos dos fármacos
Úlcera Gástrica/prevenção & controle
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Anti-Inflamatórios não Esteroides/efeitos adversos
Anti-Inflamatórios não Esteroides/uso terapêutico
Antiulcerosos/efeitos adversos
Antiulcerosos/uso terapêutico
Caspase 3/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/etiologia
Quimiocinas CXC/metabolismo
Citoproteção
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Mucosa Gástrica/efeitos dos fármacos
Mucosa Gástrica/metabolismo
Mucosa Gástrica/patologia
Glucosefosfato Desidrogenase/metabolismo
Seres Humanos
Indometacina/efeitos adversos
Interferon gama/metabolismo
Interleucina-1beta/metabolismo
Masculino
Dor/tratamento farmacológico
Peroxidase/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ranitidina/efeitos adversos
Ranitidina/uso terapêutico
Ratos
Ratos Wistar
Úlcera Gástrica/induzido quimicamente
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Anti-Ulcer Agents); 0 (Antioxidants); 0 (Bcl2 protein, rat); 0 (Chemokines, CXC); 0 (Gm1960 protein, rat); 0 (Interleukin-1beta); 0 (Proto-Oncogene Proteins c-bcl-2); 82115-62-6 (Interferon-gamma); 884KT10YB7 (Ranitidine); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 1.11.1.7 (Peroxidase); EC 3.4.22.- (Caspase 3); WYQ7N0BPYC (Acetylcysteine); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170117
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0442


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[PMID]:27858108
[Au] Autor:Flanagan T; Martin P; Gillen M; Mathews D; Lisbon E; Kruusmägi M
[Ad] Endereço:AstraZeneca Pharmaceuticals, Alderley Park, Macclesfield, Cheshire, SK10 4TF, UK.
[Ti] Título:Effects of ranitidine (antacid), food, and formulation on the pharmacokinetics of fostamatinib: results from five phase I clinical studies.
[So] Source:Eur J Clin Pharmacol;73(2):185-195, 2017 Feb.
[Is] ISSN:1432-1041
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Fostamatinib is an orally dosed phosphate prodrug that is cleaved by intestinal alkaline phosphatase to the active metabolite R406. Clinical studies were performed to assess the effect of food and ranitidine on exposure, to support in vitro-in vivo relationships (IVIVR) understanding and formulation transitions and to investigate absolute oral bioavailability. METHODS: A series of in vitro dissolution and clinical pharmacokinetic studies were performed to support the design and introduction of a new formulation, understand the impact of changes in in vitro dissolution on in vivo performance for two fostamatinib formulations, to characterize the effects of food and ranitidine on exposure, and determine the absolute oral bioavailability. RESULTS: The in vivo performance of fostamatinib was generally insensitive to changes in in vitro dissolution performance, although marked slowing of the dissolution rate did impact exposures. Food and ranitidine had minor effects on R406 exposure that were not considered clinically relevant. The absolute oral bioavailability of fostamatinib was 54.6 %. CONCLUSIONS: The absolute oral bioavailability of fostamatinib was ~55 %. Food and ranitidine had minor effects on R406 exposure. An in vitro dissolution versus clinical performance relationship was determined that supported formulation transitions.
[Mh] Termos MeSH primário: Antiácidos/farmacologia
Antiulcerosos/farmacologia
Oxazinas/farmacocinética
Pró-Fármacos/farmacocinética
Piridinas/farmacocinética
Ranitidina/farmacologia
[Mh] Termos MeSH secundário: Administração Oral
Adolescente
Adulto
Antiácidos/química
Antiulcerosos/química
Disponibilidade Biológica
Celulose/química
Química Farmacêutica
Estudos Cross-Over
Interações Medicamentosas
Feminino
Alimentos
Seres Humanos
Masculino
Meia-Idade
Oxazinas/sangue
Piridinas/sangue
Ranitidina/química
Solubilidade
Quinase Syk/antagonistas & inibidores
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antacids); 0 (Anti-Ulcer Agents); 0 (Oxazines); 0 (Prodrugs); 0 (Pyridines); 884KT10YB7 (Ranitidine); 9004-34-6 (Cellulose); EC 2.7.10.2 (Syk Kinase); OP1R32D61U (microcrystalline cellulose); SQ8A3S5101 (fostamatinib)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1007/s00228-016-2156-4



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