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[PMID]:28985539
[Au] Autor:Naidoo V; Taggart MA; Duncan N; Wolter K; Chipangura J; Green RE; Galligan TH
[Ad] Endereço:Department of Paraclinical Sciences, Faculty of Veterinary Science, University of Pretoria, South Africa; Biomedical Research Centre, Faculty of Veterinary Science, University of Pretoria, South Africa. Electronic address: vinny.naidoo@up.ac.za.
[Ti] Título:The use of toxicokinetics and exposure studies to show that carprofen in cattle tissue could lead to secondary toxicity and death in wild vultures.
[So] Source:Chemosphere;190:80-89, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Veterinary medicines can be extremely damaging to the environment, as seen with the catastrophic declines in Gyps vulture in South Asia due to their secondary exposure to diclofenac in their primary food source. Not surprisingly, concern has been raised over other similar drugs. In this study, we evaluate the toxicity of carprofen to the Gyps vulture clade through plasma pharmacokinetics evaluations in Bos taurus cattle (their food source) and Gyps africanus (a validated model species); tissue residues in cattle; and the effect of carprofen as a secondary toxicant as both tissue-bound residue or pure drug at levels expected in cattle tissues. Carprofen residues were highest in cattle kidney (7.72 ± 2.38 mg/kg) and injection site muscle (289.05 ± 98.96 mg/kg of dimension of 5 × 5 × 5 cm). Vultures exposed to carprofen as residues in the kidney tissue or pure drug equivalents showed no toxic signs. When exposed to average injection site concentrations (64 mg/kg) one of two birds died with evidence of severe renal and liver damage. Toxicokinetic analysis revealed a prolonged drug half-life of 37.75 h in the dead bird as opposed to 13.99 ± 5.61 h from healthy birds dosed intravenously at 5 mg/kg. While carprofen may generally be harmless to Gyps vultures, its high levels at the injection site in treated cattle can result in lethal exposure in foraging vultures, due to relative small area of tissue it is found therein. We thus suggest that carprofen not be used in domesticated ungulates in areas where carcasses are accessible or provided to vultures at supplementary feeding sites.
[Mh] Termos MeSH primário: Carbazóis/toxicidade
Falconiformes
Drogas Veterinárias/toxicidade
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/farmacocinética
Anti-Inflamatórios não Esteroides/toxicidade
Ásia
Carbazóis/farmacocinética
Bovinos
Morte
Diclofenaco/farmacocinética
Diclofenaco/toxicidade
Meia-Vida
Rim/efeitos dos fármacos
Rim/patologia
Fígado/efeitos dos fármacos
Fígado/patologia
Toxicocinética
Drogas Veterinárias/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Carbazoles); 0 (Veterinary Drugs); 144O8QL0L1 (Diclofenac); FFL0D546HO (carprofen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


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[PMID]:29292933
[Au] Autor:Ringbom T; Salin K; Scholz B; Hillver SE; Ljung R
[Ti] Título:Tonvis med diklofenak i våra vatten ­ regeländring behövs..
[So] Source:Lakartidningen;114, 2017 11 17.
[Is] ISSN:1652-7518
[Cp] País de publicação:Sweden
[La] Idioma:swe
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/análise
Diclofenaco/análise
Legislação de Medicamentos
Qualidade da Água/normas
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/metabolismo
Diclofenaco/metabolismo
Prescrições de Medicamentos
Uso de Medicamentos
Seres Humanos
Suécia
Águas Residuais/análise
Poluentes Químicos da Água/análise
Poluentes Químicos da Água/metabolismo
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Waste Water); 0 (Water Pollutants, Chemical); 144O8QL0L1 (Diclofenac)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE


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[PMID]:29203276
[Au] Autor:Lazarska KE; Dekker SJ; Vermeulen NPE; Commandeur JNM
[Ad] Endereço:AIMMS-Division of Molecular Toxicology, Department of Chemistry and Pharmaceutical sciences, Vrije Universiteit, De Boelelaan 1108, 1081 HZ, Amsterdam, The Netherlands.
[Ti] Título:Effect of UGT2B7*2 and CYP2C8*4 polymorphisms on diclofenac metabolism.
[So] Source:Toxicol Lett;284:70-78, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The use of diclofenac is associated with rare but severe drug-induced liver injury (DILI) in a very small number of patients. The factors which predispose susceptible patients to hepatotoxicity of diclofenac are still incompletely understood. Formation of protein-reactive metabolites by UDP-glucuronosyl transferases and cytochromes P450 is commonly considered to play an important role, as indicated by the detection of covalent protein adducts and antibodies in the serum of patients suffering from diclofenac-induced liver injury. Since no associations have been found with HLA-alleles, polymorphisms of genes encoding for proteins involved in the disposition of diclofenac may be important. Previous association studies showed that possession of the UGT2B7*2 and CYP2C8*4 alleles is more common in cases of diclofenac-induced DILI. In the present study, the metabolism of diclofenac by UGT2B7*2 and CYP2C8*4 was compared with their corresponding wild-type enzymes. Enzyme kinetic analysis revealed that recombinant UGT2B7*2 showed an almost 6-fold lower intrinsic clearance of diclofenac glucuronidation compared to UGT2B7*1. The mutant CYP2C8*4 showed approximately 35% reduced activity in the 4'-hydroxylation of diclofenac acyl glucuronide. Therefore, a decreased hepatic exposure to diclofenac acyl glucuronide is expected in patients with the UGT2B7*2 genotype. The increased risk for hepatotoxicity, therefore, might be the result from a shift to oxidative bioactivation to cytotoxic quinoneimines.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/metabolismo
Citocromo P-450 CYP2C8/genética
Diclofenaco/metabolismo
Glucuronosiltransferase/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Escherichia coli/genética
Glucuronídeos/metabolismo
Hidroxilação
Cinética
Mutação
Oxirredução
Proteínas Recombinantes
Células Sf9
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Glucuronides); 0 (Recombinant Proteins); 144O8QL0L1 (Diclofenac); EC 1.14.14.1 (CYP2C8 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP2C8); EC 2.4.1.- (UGT2B7 protein, human); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:29320568
[Au] Autor:Feng X; Tian M; Zhang W; Mei H
[Ad] Endereço:Department of Nephrology and Rheumatology, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou, China.
[Ti] Título:Gastrointestinal safety of etoricoxib in osteoarthritis and rheumatoid arthritis: A meta-analysis.
[So] Source:PLoS One;13(1):e0190798, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To ascertain if etoricoxib increases the risk of gastrointestinal adverse events (GAEs) compared with placebo, diclofenac, and naproxen in the treatment of patients with osteoarthritis (OA) or rheumatoid arthritis (RA). METHODS: Studies were searched in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials from inception to August 2017. Randomized Clinical Trials (RCTs) that compared etoricoxib with placebo and other active drug for patients with OA or RA and reported data on gastrointestinal safety (which is of interest to patients and clinicians) were included. The follow-up time window for GAEs was defined as within 28 days subsequent to the last dose of study medication. A meta-analysis was conducted using a fixed-effect model. Risk ratios (RRs) and 95% confidence intervals (CIs) were measured. RESULTS: We found nine randomized clinical trials (RCTs) that included information on gastrointestinal safety during follow-up time. Among them, five RCTs compared etoricoxib with placebo, four RCTs compared etoricoxib with diclofenac, and three RCTs compared etoricoxib with naproxen. Etoricoxib did not increase the risk of GAEs compared with placebo. Compared with diclofenac and naproxen, etoricoxib reduced the GAE risk (RR, 0.67; 95% CI, 0.59-0.76; p < 0.00001; 0.59; 0.48-0.72; < 0.00001) during follow-up time. CONCLUSIONS: In patients with OA or RA, etoricoxib did not increase the GAE risk compared with placebo, but reduced the GAE risk effectively compared with diclofenac and naproxen during follow-up time.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/efeitos adversos
Artrite Reumatoide/tratamento farmacológico
Inibidores de Ciclo-Oxigenase 2/efeitos adversos
Osteoartrite/tratamento farmacológico
Piridinas/efeitos adversos
Sulfonas/efeitos adversos
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/uso terapêutico
Inibidores de Ciclo-Oxigenase 2/uso terapêutico
Diclofenaco/efeitos adversos
Diclofenaco/uso terapêutico
Seres Humanos
Naproxeno/efeitos adversos
Naproxeno/uso terapêutico
Piridinas/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Sulfonas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase 2 Inhibitors); 0 (Pyridines); 0 (Sulfones); 144O8QL0L1 (Diclofenac); 57Y76R9ATQ (Naproxen); WRX4NFY03R (etoricoxib)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190798


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[PMID]:29068980
[Au] Autor:Li C; Qu J
[Ad] Endereço:Department of Orthopedics, The Second Hospital of Jilin University, Changchun, P. R. China.
[Ti] Título:Efficacy of dexmedetomidine for pain management in knee arthroscopy: A systematic review and meta-analysis.
[So] Source:Medicine (Baltimore);96(43):e7938, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dexmedetomidine showed some potential in pain control in patients undergoing knee arthroscopy. We conducted a systematic review and meta-analysis to explore the efficacy of dexmedetomidine in patients undergoing knee arthroscopy. METHODS: We searched the randomized controlled trials (RCTs) assessing the effect of dexmedetomidine on knee arthroscopy in PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases. The primary outcome was pain scores. Meta-analysis was performed using the random-effect model. RESULTS: Five RCTs were included. Overall, compared with control intervention in patients with knee arthroscopy, dexmedetomidine intervention could significantly reduce the pain scores [Std. mean difference = -0.84; 95% confidence interval (95% CI) = -1.24 to -0.44; P < .0001] and postoperative diclofenac sodium consumption (Std. mean difference = -1.76; 95% CI = -3.32 to -0.21; P = .03), improve duration of analgesic effect (Std. mean difference = 1.78; 95% CI = 0.56-3.00; P = .004), but showed no influence on hypotension [risk ratio (RR) = 0.93; 95% CI = 0.14-5.92; P = .94], bradycardia (RR = 4.93; 95% CI = 0.91-26.58; P = .06), nausea, and vomiting (RR = 1.96; 95% CI = 0.31-12.58; P = .48). CONCLUSION: Dexmedetomidine intervention was able to significantly reduce the pain scores and postoperative diclofenac sodium consumption, and improve duration of analgesic effect in patients undergoing knee arthroscopy, but had no influence on hypotension, bradycardia, nausea, and vomiting.
[Mh] Termos MeSH primário: Analgésicos não Entorpecentes/uso terapêutico
Artroplastia do Joelho/efeitos adversos
Dexmedetomidina/uso terapêutico
Dor Pós-Operatória/tratamento farmacológico
[Mh] Termos MeSH secundário: Analgésicos não Entorpecentes/efeitos adversos
Anti-Inflamatórios não Esteroides/administração & dosagem
Dexmedetomidina/efeitos adversos
Diclofenaco/administração & dosagem
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Anti-Inflammatory Agents, Non-Steroidal); 144O8QL0L1 (Diclofenac); 67VB76HONO (Dexmedetomidine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171026
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007938


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[PMID]:28960974
[Au] Autor:Sun R; Shi F; Liu K; Fu L; Tian C; Yang Y; Tallman KA; Porter NA; Yang J
[Ad] Endereço:State Key Laboratory of Proteomics, National Center for Protein Sciences, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine , Beijing 102206, China.
[Ti] Título:A Chemoproteomic Platform To Assess Bioactivation Potential of Drugs.
[So] Source:Chem Res Toxicol;30(10):1797-1803, 2017 Oct 16.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactive metabolites (RM) formed from bioactivation of drugs can covalently modify liver proteins and cause mechanism-based inactivation of major cytochrome P450 (CYP450) enzymes. Risk of bioactivation of a test compound is routinely examined as part of lead optimization efforts in drug discovery. Here we described a chemoproteomic platform to assess in vitro and in vivo bioactivation potential of drugs. This platform enabled us to determine reactivity of thousands of proteomic cysteines toward RMs of diclofenac formed in human liver microsomes and living animals. We pinpointed numerous reactive cysteines as the targets of RMs of diclofenac, including the active (heme-binding) sites on several key CYP450 isoforms (1A2, 2E1 and 3A4 for human, 2C39 and 3A11 for mouse). This general platform should be applied to other drugs, drug candidates, and xenobiotics with potential hepatoxicity, including environmental organic substances, bioactive natural products, and traditional Chinese medicine.
[Mh] Termos MeSH primário: Inibidores das Enzimas do Citocromo P-450/efeitos adversos
Sistema Enzimático do Citocromo P-450/metabolismo
Diclofenaco/efeitos adversos
Microssomos Hepáticos/efeitos dos fármacos
Proteômica
Xenobióticos/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Inibidores das Enzimas do Citocromo P-450/metabolismo
Diclofenaco/metabolismo
Relação Dose-Resposta a Droga
Seres Humanos
Camundongos
Microssomos Hepáticos/metabolismo
Xenobióticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochrome P-450 Enzyme Inhibitors); 0 (Xenobiotics); 144O8QL0L1 (Diclofenac); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00183


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[PMID]:28859143
[Au] Autor:Damps T; Laskowska AK; Kowalkowski T; Prokopowicz M; Puszko AK; Sosnowski P; Czuwara J; Konop M; Rózycki K; Borkowska JK; Misicka A; Rudnicka L
[Ad] Endereço:Department of Neuropeptides, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
[Ti] Título:The effect of wool hydrolysates on squamous cell carcinoma cells in vitro. Possible implications for cancer treatment.
[So] Source:PLoS One;12(8):e0184034, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Squamous cell carcinoma of the skin is the second most common cutaneous malignancy. Despite various available treatment methods and advances in noninvasive diagnostic techniques, the incidence of metastatic cutaneous squamous cell carcinoma is rising. Deficiency in effective preventive or treatment methods of transformed keratinocytes leads to necessity of searching for new anticancer agents. The present study aims to evaluate the possibility of using wool hydrolysates as such agents. Commercially available compounds such as 5-fluorouracil, ingenol mebutate, diclofenac sodium salt were also used in this study. The process of wool degradation was based on chemical pre-activation and enzymatic digestion of wool. The effect of mentioned compounds on cell viability of squamous carcinoma cell line and healthy keratinocytes was evaluated. The obtained data show a significantly stronger effect of selected wool hydrolysates compared to commercial compounds (p<0.05) on viability of cells. The wool hydrolysates decreased squamous cell carcinoma cells viability by up to 67% comparing to untreated cells. These results indicate bioactive properties of wool hydrolysates, which affect the viability of squamous carcinoma cells and decrease their number. We hypothesize that these agents may be used topically for treatment of transformed keratinocytes in actinic keratosis and invasive squamous skin cancer in humans.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/tratamento farmacológico
Hidrolisados de Proteína/química
Neoplasias Cutâneas/tratamento farmacológico
/química
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Diclofenaco/farmacologia
Diterpenos/farmacologia
Fluoruracila/farmacologia
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/patologia
Hidrolisados de Proteína/farmacologia
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-ingenyl angelate); 0 (Antineoplastic Agents); 0 (Diterpenes); 0 (Protein Hydrolysates); 144O8QL0L1 (Diclofenac); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184034


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[PMID]:28739304
[Au] Autor:El-Gowelli HM; Ibrahim KS; El-Yazbi AF; El-Mas MM
[Ad] Endereço:Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt.
[Ti] Título:Role of NADPHox/Rho-kinase signaling in the cyclosporine-NSAIDs interactions on blood pressure and baroreflexes in female rats.
[So] Source:Life Sci;185:15-22, 2017 Sep 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The hypertensive effect of the immunosuppressant drug cyclosporine (CSA) is paralleled, and probably triggered, by impaired arterial baroreceptor sensitivity (BRS). Here we asked if these effects of CSA are influenced by co-administration of nonsteroidal antiinflammatory drugs (NSAIDs) and if the oxidative NADPH-oxidase (NADPHox)/Rho-kinase (ROCK) pathway mediates this interaction. MATERIALS AND METHODS: Female rats were treated for 10days with CSA (25mg/kg/day), diclofenac (DIC, COX-1/COX-2 inhibitor, 1mg/kg/day), celecoxib (COX-2 inhibitor, 10mg/kg/day), or their combinations. Baroreflex curves relating changes in heart rate (HR) to increases or decreases in blood pressure (BP) evoked by phenylephrine (PE) and sodium nitroprusside (SNP), respectively, were constructed and slopes of the curves were taken as measures of BRS. KEY FINDINGS: Compared with control rats, CSA increased BP and reduced reflex chronotropic responses as indicated by the significantly smaller BRS and BRS values. Similar effects were observed in rats treated with diclofenac alone or combined with CSA. Whereas CSA hypertension was maintained after selective COX-2 inhibition by celecoxib, the concomitant BRS reductions were largely eliminated. NADPHox inhibition by diphenyleneiodonium (DPI) blunted the CSA/DIC-evoked increases and decreases in BP and BRS , respectively. By contrast, fasudil (ROCK inhibitor) had no effect on CSA/DIC hypertension but reversed the associated reductions in both BRS and BRS . SIGNIFICANCE: Depending on the nature of the cardiovascular response, NADPHox and ROCK contribute variably to the worsened cardiovascular profile in CSA/DIC-treated rats. Further, celecoxib rather than diclofenac could be a better choice as an add-on therapy to CSA in autoimmune arthritic conditions.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/toxicidade
Celecoxib/toxicidade
Ciclosporina/toxicidade
Diclofenaco/toxicidade
Hipertensão/induzido quimicamente
[Mh] Termos MeSH secundário: 1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/análogos & derivados
1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/farmacologia
Animais
Anti-Inflamatórios não Esteroides/administração & dosagem
Barorreflexo/efeitos dos fármacos
Pressão Sanguínea/efeitos dos fármacos
Celecoxib/administração & dosagem
Ciclosporina/administração & dosagem
Diclofenaco/administração & dosagem
Interações Medicamentosas
Feminino
NADPH Oxidases/metabolismo
Fenilefrina/farmacologia
Ratos
Ratos Wistar
Quinases Associadas a rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 144O8QL0L1 (Diclofenac); 1WS297W6MV (Phenylephrine); 83HN0GTJ6D (Cyclosporine); 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine); EC 1.6.3.- (NADPH Oxidases); EC 2.7.11.1 (rho-Associated Kinases); JCX84Q7J1L (Celecoxib); Q0CH43PGXS (fasudil)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28718684
[Au] Autor:Jain S; Ghanghas P; Rana C; Sanyal SN
[Ad] Endereço:a Department of Biophysics , Panjab University , Chandigarh , India.
[Ti] Título:Role of GSK-3ß in Regulation of Canonical Wnt/ß-catenin Signaling and PI3-K/Akt Oncogenic Pathway in Colon Cancer.
[So] Source:Cancer Invest;35(7):473-483, 2017 Aug 09.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-steroidal anti-inflammatory drugs (NSAIDs) are emerging as novel chemopreventive agents because of their ability in blocking cellular proliferation, and thereby tumor development, and also by promoting apoptosis. GSK-3ß, a serine threonine kinase and a negative regulator of the oncogenic Wnt/ß-catenin signaling pathway, plays a critical role in the regulation of oncogenesis. Celecoxib and etoricoxib, the two cyclooxygenase-2 (COX-2) selective NSAIDs, and Diclofenac, a preferential COX-2 inhibitory NSAID, had shown uniformly the chemopreventive and anti-neoplastic effects in the early stage of colon cancer by promoting apoptosis as well as an over-expression of GSK-3ß while down-regulating the PI3-K/Akt oncogenic pathway.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Transformação Celular Neoplásica/efeitos dos fármacos
Colo/efeitos dos fármacos
Neoplasias do Colo/prevenção & controle
Inibidores de Ciclo-Oxigenase 2/farmacologia
Glicogênio Sintase Quinase 3 beta/metabolismo
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Via de Sinalização Wnt/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1,2-Dimetilidrazina
Animais
Apoptose/efeitos dos fármacos
Celecoxib/farmacologia
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Colo/enzimologia
Colo/patologia
Neoplasias do Colo/induzido quimicamente
Neoplasias do Colo/enzimologia
Neoplasias do Colo/patologia
Diclofenaco/farmacologia
Feminino
PTEN Fosfo-Hidrolase/metabolismo
Piridinas/farmacologia
Ratos Sprague-Dawley
Sulfonas/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Cyclooxygenase 2 Inhibitors); 0 (Pyridines); 0 (Sulfones); 144O8QL0L1 (Diclofenac); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Gsk3b protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, rat); IX068S9745 (1,2-Dimethylhydrazine); JCX84Q7J1L (Celecoxib); WRX4NFY03R (etoricoxib)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1337783


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[PMID]:28717109
[Au] Autor:Ogihara T; Arakawa H; Jomura T; Idota Y; Koyama S; Yano K; Kojima H
[Ad] Endereço:Laboratory of Biopharmaceutics, Department of Pharmacology, Faculty of Pharmacy, Takasaki University of Health and Welfare.
[Ti] Título:Utility of human hepatocyte spheroids without feeder cells for evaluation of hepatotoxicity.
[So] Source:J Toxicol Sci;42(4):499-507, 2017.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We investigated the utility of three-dimensionally cultured hepatocytes (spheroids) without feeder cells (Sph(f-)) for the prediction of drug-induced liver injury (DILI) in humans. Sph(f-) and spheroids cultured on feeder cells (Sph(f+)) were exposed to the hepatotoxic drugs flutamide, diclofenac, isoniazid and chlorpromazine at various concentrations for 14 days, and albumin secretion and cumulative leakages of toxicity marker enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and γ-glutamyl transpeptidase (γ-GTP), were measured. The cumulative AST, LDH or γ-GTP leakages from Sph(f-) were similar to or greater than those from Sph(f+) for all drugs tested, although ALT leakages showed no consistent difference between Sph(f+) and Sph(f-). In the case of Sph(f-), significant correlations among all the toxicity markers except for γ-GTP were observed. As regards the drug concentrations causing 1.2-fold elevation of enzyme leakage (F ), no consistent difference between Sph(f+) and Sph(f-) was found, although several F values were undetermined, especially in Sph(f+). The IC of albumin secretion and F of AST leakage from Sph(f-) were equal to or lower than those of Sph(f+) for all the tested drugs. These results indicate that feeder cells might contribute to resistance to hepatotoxicity, suggesting DILI could be evaluated more accurately by using Sph(f-). We suggest that long-term exposure of Sph(f-) to drugs might be a versatile method to predict and reproduce clinical chronic toxicity, especially in response to repeated drug administration.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/etiologia
Clorpromazina/toxicidade
Diclofenaco/toxicidade
Flutamida/toxicidade
Hepatócitos/citologia
Isoniazida/toxicidade
Esferoides Celulares
Testes de Toxicidade/métodos
[Mh] Termos MeSH secundário: Alanina Transaminase/metabolismo
Albuminas/secreção
Aspartato Aminotransferases/metabolismo
Células Cultivadas
Células Alimentadoras
Seres Humanos
L-Lactato Desidrogenase/metabolismo
Fígado/efeitos dos fármacos
Fígado/enzimologia
Fígado/secreção
Fatores de Tempo
gama-Glutamiltransferase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Albumins); 144O8QL0L1 (Diclofenac); 76W6J0943E (Flutamide); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.3.2.2 (gamma-Glutamyltransferase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); U42B7VYA4P (Chlorpromazine); V83O1VOZ8L (Isoniazid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.2131/jts.42.499



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