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[PMID]:27773935
[Au] Autor:Meng Q; Duan XP; Wang CY; Liu ZH; Sun PY; Huo XK; Sun HJ; Peng JY; Liu KX
[Ad] Endereço:Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian 116044, China.
[Ti] Título:Alisol B 23-acetate protects against non-alcoholic steatohepatitis in mice via farnesoid X receptor activation.
[So] Source:Acta Pharmacol Sin;38(1):69-79, 2017 Jan.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alisol B 23-acetate (AB23A) is a natural triterpenoid isolated from the traditional Chinese medicine rhizoma alismatis, which exhibits a number of pharmacological activities, including anti-hepatitis virus, anti-cancer and antibacterial effects. In this study we examined whether AB23A protected against non-alcoholic steatohepatitis (NASH) in mice, and the mechanisms underlying the protective effects. NASH was induced in mice fed a methionine and choline-deficient (MCD) diet for 4 weeks. The mice were simultaneously treated with AB23A (15, 30, and 60 mg·kg ·d , ig) for 4 weeks. On the last day, blood samples and livers were collected. Serum liver functional enzymes, inflammatoru markers were assessed. The livers were histologically examined using H&E, Oil Red O, Masson's trichrome and Sirius Red staining. Mouse primary hepatocytes were used for in vitro experiments. The mechanisms underlying AB23A protection were analyzed using siRNA, qRT-PCR, and Western blot assays. AB23A treatment significantly and dose-dependently decreased the elevated levels of serum ALT and AST in MCD diet-fed mice. Furthermore, AB23A treatment significantly reduced hepatic triglyceride accumulation, inflammatory cell infiltration and hepatic fibrosis in the mice. AB23A-induced decreases in serum and hepatic lipids were related to decreased hepatic lipogenesis through decreasing hepatic levels of SREBP-1c, FAS, ACC1 and SCD1 and increased lipid metabolism via inducing PPARα, CPT1α, ACADS and LPL. The reduction in inflammatory cell infiltration corresponded to deceased serum levels of mKC and MCP-1 and decreased hepatic gene expression of MCP-1 and VCAM-1. The reduction in hepatic fibrosis was correlated with decreased hepatic gene expression of fibrosis markers. The protective effects of AB23A were FXR-dependent, because treatment with the FXR agonist CDCA mimicked AB23A-induced hepato-protection in the mice, whereas co-administration of FXR antagonist guggulsterone abrogated AB23A-induced hepato-protection. In mouse primary hepatocytes, FXR gene silencing abrogated AB23A-induced changes in gene expression of Apo C-II, CPT1α, ACADS and LPL. AB23A produces protective effects against NASH in mice via FXR activation.
[Mh] Termos MeSH primário: Colestenonas/farmacologia
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Receptores Citoplasmáticos e Nucleares/agonistas
[Mh] Termos MeSH secundário: Animais
Ácido Quenodesoxicólico/farmacologia
Colestenonas/antagonistas & inibidores
Deficiência de Colina
Relação Dose-Resposta a Droga
Fibrose/patologia
Expressão Gênica/efeitos dos fármacos
Hepatócitos/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Lipogênese/efeitos dos fármacos
Fígado/enzimologia
Fígado/metabolismo
Fígado/patologia
Masculino
Metionina/deficiência
Camundongos
Pregnenodionas/farmacologia
Cultura Primária de Células
Substâncias Protetoras/farmacologia
Receptores Citoplasmáticos e Nucleares/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholestenones); 0 (Pregnenediones); 0 (Protective Agents); 0 (Receptors, Cytoplasmic and Nuclear); 0 (alisol B 23-acetate); 0 (farnesoid X-activated receptor); 0GEI24LG0J (Chenodeoxycholic Acid); A4PW148END (pregna-4,17-diene-3,16-dione); AE28F7PNPL (Methionine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2016.119


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[PMID]:28552338
[Au] Autor:Lee D; Kim T; Kim KH; Ham J; Jang TS; Kang KS; Lee JW
[Ad] Endereço:College of Korean Medicine, Gachon University, Seonngman 13120, Republic of Korea; School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea.
[Ti] Título:Evaluation of guggulsterone derivatives as novel kidney cell protective agents against cisplatin-induced nephrotoxicity.
[So] Source:Bioorg Med Chem Lett;27(14):3156-3161, 2017 07 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Guggulsterone derivatives were prepared using [3+2] click chemistry with aryl and alkyl acetylene. The series of derivatives were evaluated for their cellular protective effects on cisplatin-treated cultured LLC-PK1 kidney epithelial cells. Among the guggulsterone-triazole derivatives, compound 6g, which contains a hydroxyl methyl group, was the most active of all the derivatives. In an additional study, we determined that inhibition of the mitogen-activated protein kinase/caspase-3 signaling cascade by 6g mediates its protective effects against cytotoxicity in cultured LLC-PK1 cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Pregnenodionas/química
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Caspase 3/química
Caspase 3/metabolismo
Cisplatino/farmacologia
Química Click
Rim/citologia
Rim/efeitos dos fármacos
Rim/metabolismo
Células LLC-PK1
Microscopia
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Pregnenodionas/farmacologia
Substâncias Protetoras/química
Transdução de Sinais/efeitos dos fármacos
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Pregnenediones); 0 (Protective Agents); A4PW148END (pregna-4,17-diene-3,16-dione); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


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[PMID]:28329498
[Au] Autor:Ferreira BR; Vaz AS; Ramos L; Reis JP; Gonçalo M
[Ad] Endereço:Department of Dermatology, Coimbra Hospital and University Centre, Coimbra, Portugal. barbara.roqueferreira@gmail.com.
[Ti] Título:Bullous pemphigoid of infancy - report and review of infantile and pediatric bullous pemphigoid.
[So] Source:Dermatol Online J;23(2), 2017 Feb 16.
[Is] ISSN:1087-2108
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A 4-month-old infant was observed with an acute itchy bullous dermatosis, predominantly involving the extremities, which revealed a dermal infiltrate rich in eosinophils, C3 deposits at the dermalepidermal junction, and circulating antibodies to BP180 antigen, confirming the diagnosis of bullous pemphigoid. He was initially treated with deflazacort 1 mg/kg/day, further increased to 2 mg/ kg/day, followed by reduction over seven weeks with complete clinical resolution within this period. We discuss epidemiology, etiology, relationship with vaccination, clinical features, and treatment of thisrelatively rare bullous dermatosis in the pediatric age.
[Mh] Termos MeSH primário: Penfigoide Bolhoso/diagnóstico
[Mh] Termos MeSH secundário: Anti-Inflamatórios/uso terapêutico
Autoanticorpos/imunologia
Autoantígenos/imunologia
Complemento C3/imunologia
Ensaio de Imunoadsorção Enzimática
Técnica Direta de Fluorescência para Anticorpo
Técnica Indireta de Fluorescência para Anticorpo
Seres Humanos
Lactente
Masculino
Colágenos não Fibrilares/imunologia
Penfigoide Bolhoso/tratamento farmacológico
Penfigoide Bolhoso/imunologia
Penfigoide Bolhoso/patologia
Pregnenodionas/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Autoantibodies); 0 (Autoantigens); 0 (Complement C3); 0 (Non-Fibrillar Collagens); 0 (Pregnenediones); 0 (collagen type XVII); KR5YZ6AE4B (deflazacort)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


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[PMID]:28189974
[Au] Autor:Zuska-Prot M; Maslanka T
[Ad] Endereço:Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowskiego Street 13, 10-719 Olsztyn, Poland. Electronic address: monika.zuska@gmail.com.
[Ti] Título:Effect of inhaled and systemic glucocorticoid treatment on CD4 regulatory and effector T cells in a mouse model of allergic asthma.
[So] Source:Int Immunopharmacol;45:98-109, 2017 Apr.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To achieve a better understanding of mechanisms underlying the anti-asthmatic action of inhaled and systemic glucocorticoids (GCs) and to provide more data regarding the risk of a negative effect of inhaled GCs on CD4 T cells, a study was conducted on the effect of ciclesonide and methylprednisolone on CD4 effector (Teff), regulatory (Treg) and resting (Trest) T cells within respiratory and extra-respiratory tissues in a mouse model of allergic asthma. The study indicated that one, and possibly a key mechanism, underlying the anti-asthmatic action of inhaled and systemic GCs is the prevention of the activation and clonal expansion of CD4 Teff cells in the mediastinal lymph nodes (MLNs), which consequently prevents infiltration of the lungs with CD4 Teff cells. The beneficial effects of GCs in asthma treatment were not mediated through increased recruitment of Treg cells into the MLNs and lungs and/or local generation of Treg cells. The results demonstrated that inhaled and systemic GCs induced comparable depletion of normal CD4 Teff, Trest and Treg cells in the MLNs, head and neck lymph nodes and peripheral blood. Furthermore, inhaled, but not systemic GC therapy, led to the loss of these cells in the lungs. Thus, the study suggests that inhaled GC therapy may not be safer at all than systemic one with respect to the adverse effect on CD4 T cells present within and outside the respiratory tract. Moreover, administration of inhaled GCs can produce negative effects on lung-residing CD4 T cells.
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Asma/tratamento farmacológico
Pulmão/efeitos dos fármacos
Metilprednisolona/uso terapêutico
Pregnenodionas/uso terapêutico
Linfócitos T Auxiliares-Indutores/efeitos dos fármacos
Linfócitos T Reguladores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração por Inalação
Animais
Apoptose/efeitos dos fármacos
Células Cultivadas
Modelos Animais de Doenças
Seres Humanos
Pulmão/imunologia
Ativação Linfocitária/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Ovalbumina/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Pregnenediones); 9006-59-1 (Ovalbumin); S59502J185 (ciclesonide); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28159683
[Au] Autor:Davidson N; Tong HJ; Kalberer M; Seville PC; Ward AD; Kuimova MK; Pope FD
[Ad] Endereço:School of Geography, Earth and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
[Ti] Título:Measurement of the Raman spectra and hygroscopicity of four pharmaceutical aerosols as they travel from pressurised metered dose inhalers (pMDI) to a model lung.
[So] Source:Int J Pharm;520(1-2):59-69, 2017 Mar 30.
[Is] ISSN:1873-3476
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Particle inhalation is an effective and rapid delivery method for a variety of pharmaceuticals, particularly bronchodilation drugs used for treating asthma and COPD. Conditions of relative humidity and temperature inside the lungs are generally very different from the outside ambient air, with the lung typically being warmer and more humid. Changes in humidity, from inhaler to lung, can cause hygroscopic phase transitions and particle growth. Increasing particle size and mass can negatively affect particle deposition within the lung leading to inefficient treatment, while deliquescence prior to impaction is liable to accelerate drug uptake. To better understand the hygroscopic properties of four pharmaceutical aerosol particles; pharmaceutical particles from four commercially available pressurised metered dose inhalers (pMDIs) were stably captured in an optical trap, and their composition was examined online via Raman spectroscopy. Micron-sized particles of salbutamol sulfate, salmeterol xinafoate, fluticasone propionate and ciclesonide were levitated and examined over a range of relative humidity values inside a chamber designed to mimic conditions within the respiratory tract. The effect of temperature upon hygroscopicity was also investigated for salbutamol sulfate particles. Salbutamol sulfate was found to have significant hygroscopicity, salmeterol xinafoate showed some hygroscopic interactions, whilst fluticasone propionate and ciclesonide revealed no observable hygroscopicity. Thermodynamic and structural modelling is used to explain the observed experimental results.
[Mh] Termos MeSH primário: Aerossóis/química
Análise Espectral Raman
Molhabilidade
[Mh] Termos MeSH secundário: Albuterol/química
Fluticasona/química
Umidade
Inaladores Dosimetrados
Modelos Estruturais
Tamanho da Partícula
Pregnenodionas/química
Xinafoato de Salmeterol/química
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aerosols); 0 (Pregnenediones); 6EW8Q962A5 (Salmeterol Xinafoate); CUT2W21N7U (Fluticasone); QF8SVZ843E (Albuterol); S59502J185 (ciclesonide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170205
[St] Status:MEDLINE


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[PMID]:28043681
[Au] Autor:Wong BL; Rybalsky I; Shellenbarger KC; Tian C; McMahon MA; Rutter MM; Sawnani H; Jefferies JL
[Ad] Endereço:Comprehensive Neuromuscular Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH. Electronic address: brenda.wong@cchmc.org.
[Ti] Título:Long-Term Outcome of Interdisciplinary Management of Patients with Duchenne Muscular Dystrophy Receiving Daily Glucocorticoid Treatment.
[So] Source:J Pediatr;182:296-303.e1, 2017 Mar.
[Is] ISSN:1097-6833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate clinical outcomes and steroid side effects in a cohort of patients with Duchenne muscular dystrophy (DMD) treated with long-term daily glucocorticoid therapy. Although daily glucocorticoid therapy has been shown to extend ambulatory function in DMD, less frequent dosing is often used because of side effect concerns. STUDY DESIGN: Retrospective study of 97 patients with DMD aged 10 to <16 years treated with daily glucocorticoid (89% on deflazacort) for a mean of 8.5 years. Outcome measures were motor, pulmonary, and cardiac function, and scoliosis. Side effects were growth failure and weight gain, facial fullness, blood pressure, bone health, cataracts, gastrointestinal symptoms, behavior, hypertrichosis, and need for medication interventions. RESULTS: For 13- to 16-year-old patients, 40% could rise from the floor and 50% could perform the 30-foot run test. Forced vital capacity for the entire cohort was well preserved. Thirteen percent of younger (10- to <13-year-old) and 21% of older patients had findings of left ventricle systolic dysfunction. Six percent (all aged 16 years) developed scoliosis (Cobb angle >20 degrees). Eighty-six percent had normal weight velocities; 30% had no increased facial fullness; 72% had short stature; and 19% had asymptomatic cataracts. Asymptomatic spine compression deformities were noted in 76% and long bone fractures in 30%. One patient stopped glucocorticoid because of behavioral concerns. CONCLUSIONS: With evidence for improved outcomes and manageable side effects, we recommend use of daily glucocorticoid therapy for patients with DMD with anticipatory management of side effects and a coordinated interdisciplinary care approach.
[Mh] Termos MeSH primário: Glucocorticoides/administração & dosagem
Glucocorticoides/efeitos adversos
Distrofia Muscular de Duchenne/tratamento farmacológico
Equipe de Assistência ao Paciente/organização & administração
[Mh] Termos MeSH secundário: Adolescente
Fatores Etários
Criança
Estudos de Coortes
Relação Dose-Resposta a Droga
Esquema de Medicação
Terapia por Exercício/métodos
Seguimentos
Fraturas Ósseas/induzido quimicamente
Fraturas Ósseas/fisiopatologia
Seres Humanos
Resistência à Insulina
Assistência de Longa Duração
Masculino
Distrofia Muscular de Duchenne/diagnóstico
Distrofia Muscular de Duchenne/reabilitação
Osteoporose/induzido quimicamente
Osteoporose/fisiopatologia
Prednisona/administração & dosagem
Prednisona/efeitos adversos
Pregnenodionas/administração & dosagem
Pregnenodionas/efeitos adversos
Estudos Retrospectivos
Medição de Risco
Índice de Gravidade de Doença
Resultado do Tratamento
Ganho de Peso
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Pregnenediones); KR5YZ6AE4B (deflazacort); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE


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[PMID]:27896916
[Au] Autor:Xu W; Lu C; Zhang F; Shao J; Yao S; Zheng S
[Ad] Endereço:Department of Pharmacology, School of Pharmacy, Nanjing University of Chinese Medicine, China.
[Ti] Título:Dihydroartemisinin counteracts fibrotic portal hypertension via farnesoid X receptor-dependent inhibition of hepatic stellate cell contraction.
[So] Source:FEBS J;284(1):114-133, 2017 Jan.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Portal hypertension is a frequent pathological symptom occurring especially in hepatic fibrosis and cirrhosis. Current paradigms indicate that inhibition of hepatic stellate cell (HSC) activation and contraction is anticipated to be an attractive therapeutic strategy, because activated HSC dominantly facilitates an increase in intrahepatic vein pressure through secreting extracellular matrix and contracting. Our previous in vitro study indicated that dihydroartemisinin (DHA) inhibited contractility of cultured HSC by activating intracellular farnesoid X receptor (FXR). However, the effect of DHA on fibrosis-related portal hypertension still requires clarification. In this study, gain- and loss-of-function models of FXR in HSC were established to investigate the mechanisms underlying DHA protection against chronic CCl -caused hepatic fibrosis and portal hypertension. Immunofluorescence staining visually showed a decrease in FXR expression in CCl -administrated rat HSC but an increase in that in DHA-treated rat HSC. Serum diagnostics and morphological analyses consistently indicated that DHA exhibited hepatoprotective effects on CCl -induced liver injury. DHA also reduced CCl -caused inflammatory mediator expression and inflammatory cell infiltration. These improvements were further enhanced by INT-747 but weakened by Z-guggulsterone. Noteworthily, DHA, analogous to INT-747, significantly lowered portal vein pressure and suppressed fibrogenesis. Experiments on mice using FXR shRNA lentivirus consolidated the results above. Mechanistically, inhibition of HSC activation and contraction was found as a cellular basis for DHA to relieve portal hypertension. These findings demonstrated that DHA attenuated portal hypertension in fibrotic rodents possibly by targeting HSC contraction via a FXR activation-dependent mechanism. FXR could be a target molecule for reducing portal hypertension during hepatic fibrosis.
[Mh] Termos MeSH primário: Artemisininas/farmacologia
Células Estreladas do Fígado/efeitos dos fármacos
Hipertensão Portal/prevenção & controle
Cirrose Hepática/tratamento farmacológico
Substâncias Protetoras/farmacologia
Receptores Citoplasmáticos e Nucleares/genética
[Mh] Termos MeSH secundário: Animais
Tetracloreto de Carbono
Morte Celular/efeitos dos fármacos
Ácido Quenodesoxicólico/análogos & derivados
Ácido Quenodesoxicólico/farmacologia
Expressão Gênica
Células Estreladas do Fígado/metabolismo
Células Estreladas do Fígado/patologia
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Hipertensão Portal/induzido quimicamente
Hipertensão Portal/genética
Hipertensão Portal/patologia
Fígado/irrigação sanguínea
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Cirrose Hepática/induzido quimicamente
Cirrose Hepática/genética
Cirrose Hepática/patologia
Masculino
Camundongos
Camundongos Endogâmicos ICR
Camundongos Transgênicos
Veia Porta/efeitos dos fármacos
Pregnenodionas/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores Citoplasmáticos e Nucleares/agonistas
Receptores Citoplasmáticos e Nucleares/antagonistas & inibidores
Receptores Citoplasmáticos e Nucleares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Artemisinins); 0 (Pregnenediones); 0 (Protective Agents); 0 (Receptors, Cytoplasmic and Nuclear); 0 (farnesoid X-activated receptor); 0462Z4S4OZ (obeticholic acid); 0GEI24LG0J (Chenodeoxycholic Acid); 6A9O50735X (dihydroartemisinin); A4PW148END (pregna-4,17-diene-3,16-dione); CL2T97X0V0 (Carbon Tetrachloride)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1111/febs.13956


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[PMID]:27843100
[Au] Autor:Raju CK; Pandey AK; Ghosh K; Pola A; Goud SK; Jaywant MA; Navalgund SG; Surendranath KV
[Ad] Endereço:Analytical Research and Development, United States Pharmacopeial Convention-India (P) Ltd., Plot No. D6 & D8, IKP, Genome Valley, Shameerpet, Hyderabad,500078, India.
[Ti] Título:Isolation and structural characterization of novel photolytic degradation impurities of Deflazacort using Q-TOF, 2D-NMR and FTIR.
[So] Source:J Pharm Biomed Anal;133:82-89, 2017 Jan 30.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Forced Degradation of Deflazacort drug substance in ultraviolet light condition resulted into a number of significant degradation products. Two of these degradation products were found to be unknown during the study and marked as DD-I and DD-II. Thus, the objective of this work is to investigate and identify these two novel degradation products of DFZ. The isolation method for these new degradation products were developed using a new reverse-phase high performance liquid chromatography (HPLC). DD-I and DD-II, eluting at 0.53 and 1.57 relative retention times with respect to Deflazacort (DFZ) peak respectively, were isolated from reaction mass using preparative HPLC and their structures were elucidated using high resolution MS, multidimensional NMR and FTIR spectroscopic techniques. To best of our knowledge, these two degradation products are novel impurities which are not discussed in any form of publication yet.
[Mh] Termos MeSH primário: Oxazóis/química
Oxazóis/isolamento & purificação
Pregnenodionas/química
Pregnenodionas/isolamento & purificação
[Mh] Termos MeSH secundário: Contaminação de Medicamentos
Estrutura Molecular
Fotólise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oxazoles); 0 (Pregnenediones); KR5YZ6AE4B (deflazacort)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


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[PMID]:27639937
[Au] Autor:Milara J; Morell A; Ballester B; Armengot M; Morcillo E; Cortijo J
[Ad] Endereço:Department of Pharmacy, University Hospital Consortium, Valencia, Spain; Department of Pharmacology, Faculty of Medicine, Jaume I University, Castellon, Spain; Department of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain; CIBERES, Health Institute Carlos III, Valencia, Sp
[Ti] Título:MUC4 impairs the anti-inflammatory effects of corticosteroids in patients with chronic rhinosinusitis with nasal polyps.
[So] Source:J Allergy Clin Immunol;139(3):855-862.e13, 2017 Mar.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Current evidence suggests that membrane-tethered mucins could mediate corticosteroid efficacy, interacting with glucocorticoid receptor (GR) in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). Mucin 4 (MUC4)-tethered mucin is expressed in nasal polyp (NP) epithelial cells and upregulated under inflammatory conditions. Moreover, MUC4ß has the capacity to interact with other intracellular proteins. We hypothesized that MUC4 modulates corticosteroid efficacy of patients with CRSwNP. OBJECTIVE: We sought to analyze the role of MUC4 in corticosteroid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved. METHODS: Eighty-one patients with CRSwNP took oral corticosteroids for 15 days. Corticosteroid resistance was evaluated by using nasal endoscopy. Expression of MUC4 and MUC4ß was evaluated by means of real-time PCR, Western blotting, and immunohistochemistry. BEAS-2B knockdown with RNA interference for MUC4 (small interfering RNA [siRNA]-MUC4) was used to analyze the role of MUC4 in the anti-inflammatory effects of dexamethasone. RESULTS: Twenty-two patients had NPs resistant to oral corticosteroids. MUC4 expression was upregulated in these patients. In siRNA-MUC4 BEAS-2B airway epithelial cells dexamethasone produced higher anti-inflammatory effects, increased inhibition of phospho-extracellular signal-regulated kinase 1/2, increased mitogen-activated protein kinase phosphatase 1 expression, and increased glucocorticoid response element activation. Immunoprecipitation and immunofluorescence experiments revealed that MUC4ß forms a complex with GRα in the nuclei of NP epithelial cells from corticosteroid-resistant patients. CONCLUSION: MUC4ß participates in the corticosteroid resistance process, inhibiting normal GRα nuclear function. The high expression of MUC4 in patients with CRSwNP might participate in corticosteroid resistance.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Resistência a Medicamentos
Mucina-4/imunologia
Pólipos Nasais/tratamento farmacológico
Pregnenodionas/uso terapêutico
Rinite/tratamento farmacológico
Sinusite/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Anti-Inflamatórios/farmacologia
Linhagem Celular
Células Cultivadas
Doença Crônica
Dexametasona/farmacologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Feminino
Células HEK293
Seres Humanos
Masculino
Meia-Idade
Mucina-4/genética
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Pregnenediones); 7S5I7G3JQL (Dexamethasone); KR5YZ6AE4B (deflazacort)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160919
[St] Status:MEDLINE


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[PMID]:27522955
[Au] Autor:Lavorini F; Pedersen S; Usmani OS; Aerosol Drug Management Improvement Team (ADMIT)
[Ad] Endereço:Department of Experimental and Clinical Medicine, Careggi University Hospital, Florence, Italy. Electronic address: federico.lavorini@unifi.it.
[Ti] Título:Dilemmas, Confusion, and Misconceptions Related to Small Airways Directed Therapy.
[So] Source:Chest;151(6):1345-1355, 2017 Jun.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During the past decade, there has been increasing evidence that the small airways (ie, airways < 2 mm in internal diameter) contribute substantially to the pathophysiologic and clinical expression of asthma and COPD. The increased interest in small airways is, at least in part, a result of innovation in small-particle aerosol formulations that better target the distal lung and also advanced physiologic methods of assessing small airway responses. Increasing the precision of drug deposition may improve targeting of specific diseases or receptor locations, decrease airway drug exposure and adverse effects, and thereby increase the efficiency and effectiveness of inhaled drug delivery. The availability of small-particle aerosols of corticosteroids, bronchodilators, or their combination enables a higher total lung deposition and better peripheral lung penetration and provides added clinical benefit, compared with large-particle aerosol treatment. However, a number of questions remain unanswered about the pragmatic approach relevant for clinicians to consider the role of small airways directed therapy in the day-to-day management of asthma and COPD. We thus have tried to clarify the dilemmas, confusion, and misconceptions related to small airways directed therapy. To this end, we have reviewed all studies on small-particle aerosol therapy systematically to address the dilemmas, confusion, and misconceptions related to small airways directed therapy.
[Mh] Termos MeSH primário: Asma/tratamento farmacológico
Bronquíolos/fisiopatologia
Broncodilatadores/administração & dosagem
Glucocorticoides/administração & dosagem
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração por Inalação
Asma/fisiopatologia
Beclometasona/administração & dosagem
Gerenciamento Clínico
Combinação de Medicamentos
Inaladores de Pó Seco
Desenho de Equipamento
Fluocinolona Acetonida/administração & dosagem
Fluocinolona Acetonida/análogos & derivados
Fumarato de Formoterol/administração & dosagem
Seres Humanos
Espaçadores de Inalação
Inaladores Dosimetrados
Nebulizadores e Vaporizadores
Tamanho da Partícula
Pregnenodionas/administração & dosagem
Pressão
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bronchodilator Agents); 0 (Drug Combinations); 0 (Glucocorticoids); 0 (Pregnenediones); 0CD5FD6S2M (Fluocinolone Acetonide); KGZ1SLC28Z (Beclomethasone); QK4DYS664X (flunisolide); S59502J185 (ciclesonide); W34SHF8J2K (Formoterol Fumarate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160816
[St] Status:MEDLINE



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