Base de dados : MEDLINE
Pesquisa : D02.455.849.919.530.333 [Categoria DeCS]
Referências encontradas : 447 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 45 ir para página                         

  1 / 447 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29382005
[Au] Autor:Zhang H; Yang B
[Ad] Endereço:Department of Orthopedics, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College (CAMS & PUMC), Beijing, China.
[Ti] Título:Successful treatment of pachydermoperiostosis patients with etoricoxib, aescin, and arthroscopic synovectomy: Two case reports.
[So] Source:Medicine (Baltimore);96(47):e8865, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Pachydermoperiostosis (PDP) is a rare hereditary disorder that affects the skin and bones. PDP is characterized by periostosis, digital clubbing, and pachydermia. Previous studies demonstrated that increased prostaglandin E2 (PGE2) levels resulting from defective protein degradation pathways play a crucial role in PDP pathogenesis, and males were more commonly and severely affected than females. Moreover, nearly all PDP patients suffer from refractory arthralgia. Although several different treatment modalities are used for PDP, therapy for this disease remains challenging. PATIENTS CONCERNS: Two cases of PDP showing symptoms consistent with polyarthritis and arthralgia that mainly affected the knees and ankles. DIAGNOSES: The diagnostic criteria for PDP include digital clubbing, periostosis, and pachydermia. The 2 patients were diagnosed as PDP based on the finger clubbing, facial cutis furrowing, knee and ankle arthritis, and radiographic evidence of periosteal proliferation. INTERVENTIONS: Patient 1 had massive joint effusion that was treated by oral administration of etoricoxib and aescin combined with arthroscopic synovectomy, whereas Patient 2 had mild joint swelling and accepted only oral medication. OUTCOMES: Clinical symptoms of the 2 patients greatly improved after the treatment. During the 1-year follow-up, the patient experienced no adverse effects or recurrence. LESSONS: The therapeutic results showed that oral etoricoxib could reduce inflammation and retard progression of pachydermia, or even relieve facial skin furrowing, but had limited efficacy for arthralgia. However, oral aescin had satisfactory efficacy for arthralgia. Thus, etoricoxib combined with aescin is a safe and effective treatment for PDP. Meanwhile, arthroscopic synovectomy can be used to treat joint effusion, but had no therapeutic effect on arthralgia. Therefore, postoperative oral medications would be needed as subsequent therapy for joint problems. In conclusion, this study proposes an effective and safe treatment plan to address symptoms experienced by PDP patients.
[Mh] Termos MeSH primário: Fármacos Cardiovasculares/administração & dosagem
Inibidores de Ciclo-Oxigenase 2/administração & dosagem
Escina/administração & dosagem
Osteoartropatia Hipertrófica Primária/terapia
Piridinas/administração & dosagem
Sulfonas/administração & dosagem
Sinovectomia/métodos
[Mh] Termos MeSH secundário: Artroscopia
Terapia Combinada
Seres Humanos
Masculino
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Cyclooxygenase 2 Inhibitors); 0 (Pyridines); 0 (Sulfones); 6805-41-0 (Escin); WRX4NFY03R (etoricoxib)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008865


  2 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28527823
[Au] Autor:Kim JW; Ha TK; Cho H; Kim E; Shim SH; Yang JL; Oh WK
[Ad] Endereço:Korea Bioactive Natural Material Bank, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Republic of Korea.
[Ti] Título:Antiviral escin derivatives from the seeds of Aesculus turbinata Blume (Japanese horse chestnut).
[So] Source:Bioorg Med Chem Lett;27(13):3019-3025, 2017 07 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Porcine epidemic diarrhea virus (PEDV) causes severe diarrhea and high fatality of piglets, influencing the swine industry. Japanese horse chestnut (seed of Aesculus turbinata) contains many saponin mixtures, called escins, and has been used for a long time as a traditional medicinal plant. Structure-activity relationship (SAR) studies on escins have revealed that acylations at C-21 and C-22 with angeloyl or tigloyl groups were important for their cytotoxic effects. However, the strong cytotoxicity of escins makes them hard to utilize for other diseases and to develop as nutraceuticals. In this research, we investigated whether escin derivatives 1-7 (including new compounds 2, 3, 5 and 6), without the angeloyl or tigloyl groups and with modified glycosidic linkages by hydrolysis, have PEDV inhibitory effects with less cytotoxicity. Compounds 1-7 had no cytotoxicity at 20µM on VERO cells, while compounds 8-10 showed strong cytotoxicity at similar concentrations on PEDV. Our results suggest that escin derivatives showed strong inhibitory activities on PEDV replication with lowered cytotoxicity. These studies propose a method to utilize Japanese horse chestnut for treating PEDV and to increase the diversity of its bioactive compounds.
[Mh] Termos MeSH primário: Aesculus/química
Antivirais/farmacologia
Escina/farmacologia
Vírus da Diarreia Epidêmica Suína/efeitos dos fármacos
Sementes/química
[Mh] Termos MeSH secundário: Animais
Antivirais/química
Antivirais/isolamento & purificação
Sobrevivência Celular/efeitos dos fármacos
Cercopithecus aethiops
Relação Dose-Resposta a Droga
Escina/química
Escina/isolamento & purificação
Testes de Sensibilidade Microbiana
Estrutura Molecular
Relação Estrutura-Atividade
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 6805-41-0 (Escin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE


  3 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28075477
[Au] Autor:Yuan SY; Cheng CL; Wang SS; Ho HC; Chiu KY; Chen CS; Chen CC; Shiau MY; Ou YC
[Ad] Endereço:Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung 40705, Taiwan, R.O.C.
[Ti] Título:Escin induces apoptosis in human renal cancer cells through G2/M arrest and reactive oxygen species-modulated mitochondrial pathways.
[So] Source:Oncol Rep;37(2):1002-1010, 2017 Feb.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Escin, a natural pentacyclic triterpenoid compound, exhibits antitumor effects on various types of human cancer cells, but its effect on human renal cancer cells has not been fully elucidated. In the present study, we demonstrated that escin elicits cytotoxic effects on human renal cancer cells (786-O and Caki-1) in a dose-dependent manner, as determined by MTT assay. Escin induced G2/M arrest, and then increased the sub-G1 population, Annexin V binding, activation of caspase-9/-3, cleavage of poly(ADP-ribose) polymerase (PARP) and Bax protein. Escin also decreased the anti-apoptotic protein levels of Bcl-2, X-linked inhibitor of apoptosis protein and survivin. In addition, escin induced reactive oxygen species (ROS) generation, leading to mitochondrial membrane potential dysfunction and inducing apoptosis in 786-O renal cancer cells, which were suppressed by antioxidants, such as NAC. Collectively, our results suggest that escin induces apoptosis via the intrinsic-mitochondrial apoptosis pathway through G2/M arrest and ROS generation in human renal cancer cells. Escin appears to have potential as a clinically useful chemotherapeutic agent for human renal cancer.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Escina/farmacologia
Neoplasias Renais/tratamento farmacológico
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Caspases/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Neoplasias Renais/metabolismo
Neoplasias Renais/patologia
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Reactive Oxygen Species); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 6805-41-0 (Escin); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5348


  4 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28064552
[Au] Autor:Singh H; Sidhu S; Chopra K; Khan MU
[Ad] Endereço:a Department of Research, Innovations & Consultancy , IKG Punjab Technical University , Kapurthala , Punjab , India.
[Ti] Título:The novel role of ß-aescin in attenuating CCl -induced hepatotoxicity in rats.
[So] Source:Pharm Biol;55(1):749-757, 2017 Dec.
[Is] ISSN:1744-5116
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: ß-Aescin has anti-inflammatory, anti-oxidant and antiedematous properties. OBJECTIVE: The present study investigated the hepatoprotective effect and underlying mechanisms of ß-aescin in CCl -induced liver damage. MATERIALS AND METHODS: Thirty-five Wistar rats were divided into six groups: normal control, CCl control, silymarin (50 mg/kg, p.o) and ß-aescin (0.9, 1.8 and 3.6 mg/kg, i.p.) treatment for 14 d. CCl (1 mL/kg, i.p. for 3 d) was administered to produce hepatic damage. Ponderal changes and liver marker enzymes were estimated. Hepatic oxidative and nitrosative stress was estimated by levels of thiobarbituric acid reactive substances (TBARS), glutathione (GSH) and nitrite/nitrate. Serum TGF-ß1 and TNF-α were estimated by ELISA technique. Hepatic collagen and histopathological studies were carried out. RESULTS: ß-Aescin (3.6 mg/kg) markedly decreased CCl -induced increased levels of ALT, AST, ALP (71.77 versus 206.7, 71.39 versus 171.82, 121.20 versus 259 IU/L, respectively), total bilirubin (0.41 versus 1.35 mg/dL), TBARS (2.0 versus 8.83 nmol MDA/mg protein), nitrite/nitrate (352.50 versus 745.15 µg/mL) and increased CCl -induced decreased GSH levels (0.095 versus 0.048 µmol/mg protein). ß-Aescin (3.6 mg/kg) induced focal regenerative changes in liver and markedly decreased TBARS (2.0 versus 8.83 nmol MDA/mg protein), nitrite/nitrate (352.50 versus 745.15 µg/mL), TGF-ß1 (92.28 versus 152.1 pg/mL), collagen content (110.75 versus 301.74 µmol/100 mg tissue) and TNF-α (92.82 versus 170.56 pg/mL) when compared with CCl control. DISCUSSION AND CONCLUSION: The findings suggest that ß-aescin has a protective effect on CCl -induced liver injury, exhibited via its anti-inflammatory, antioxidative, antinitrosative and antifibrotic properties inducing repair regeneration of liver. Hence, it can be used as a promising hepatoprotective agent.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico
Escina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Tetracloreto de Carbono
Colágeno/análise
Feminino
Glutationa/análise
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); 6805-41-0 (Escin); 9007-34-5 (Collagen); CL2T97X0V0 (Carbon Tetrachloride); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170131
[Lr] Data última revisão:
170131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE
[do] DOI:10.1080/13880209.2016.1275023


  5 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27858307
[Au] Autor:Filatova TS; Naumenko N; Galenko-Yaroshevsky PA; Abramochkin DV
[Ad] Endereço:Department of Human and Animal Physiology, Biological Faculty of the Moscow State University, Leninskiye Gory, 1, 12, Moscow, Russia.
[Ti] Título:M3 cholinoreceptors alter electrical activity of rat left atrium via suppression of L-type Ca current without affecting K conductance.
[So] Source:J Physiol Biochem;73(2):167-174, 2017 May.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Electrophysiological effects produced by selective activation of M3 cholinoreceptors were studied in isolated left atrium preparations from rat using the standard sharp glass microelectrode technique. The stimulation of M3 receptors was obtained by application of muscarinic agonist pilocarpine (10 M) in the presence of selective M2 antagonist methoctramine (10 M). Stimulation of M3 receptors induced marked reduction of action potential duration by 14.4 ± 2.4% and 16.1 ± 2.5% of control duration measured at 50 and 90% of repolarization, respectively. This effect was completely abolished by selective M3 blocker 4-DAMP (10 M). In isolated myocytes obtained from the rat left atrium, similar pharmacological stimulation of M3 receptors led to suppression of peak L-type calcium current by 13.9 ± 2.6% of control amplitude (measured at +10 mV), but failed to affect K currents I , I , and I . In the absence of M2 blocker methoctramine, pilocarpine (10 M) produced stronger attenuation of I and induced an increase in I . This additive inward rectifier current could be abolished by highly selective blocker of K 3.1/3.4 channels tertiapin-Q (10 M) and therefore was identified as I . Thus, in the rat atrial myocardium activation of M3 receptors leads to shortening of action potentials via suppression of I , but does not enhance the major potassium currents involved in repolarization. Joint stimulation of M2 and M3 receptors produces stronger action potential shortening due to M2-mediated activation of I
[Mh] Termos MeSH primário: Canais de Cálcio Tipo L/metabolismo
Regulação para Baixo
Átrios do Coração/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Receptor Muscarínico M3/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Animais não Endogâmicos
Canais de Cálcio Tipo L/química
Fármacos Cardiovasculares/farmacologia
Células Cultivadas
Regulação para Baixo/efeitos dos fármacos
Fenômenos Eletrofisiológicos/efeitos dos fármacos
Escina/farmacologia
Átrios do Coração/citologia
Átrios do Coração/efeitos dos fármacos
Técnicas In Vitro
Camundongos
Microeletrodos
Agonistas Muscarínicos/farmacologia
Antagonistas Muscarínicos/farmacologia
Técnicas de Patch-Clamp
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio/agonistas
Canais de Potássio/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização/agonistas
Canais de Potássio Corretores do Fluxo de Internalização/antagonistas & inibidores
Ratos
Receptor Muscarínico M3/agonistas
Receptor Muscarínico M3/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels, L-Type); 0 (Cardiovascular Agents); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 0 (Potassium Channel Blockers); 0 (Potassium Channels); 0 (Potassium Channels, Inwardly Rectifying); 0 (Receptor, Muscarinic M3); 6805-41-0 (Escin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1007/s13105-016-0538-9


  6 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27831638
[Au] Autor:Hu S; Belcaro G; Dugall M; Hosoi M; Togni S; Maramaldi G; Giacomelli L
[Ad] Endereço:Department SMO Biotech, Irvine3 Labs, Circulation Sciences, Chieti-Pescara University, Italy. lu.giacomelli6@gmail.com.
[Ti] Título:Aescin-based topical formulation to prevent foot wounds and ulcerations in diabetic microangiopathy.
[So] Source:Eur Rev Med Pharmacol Sci;20(20):4337-4342, 2016 Oct.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Impairment of the peripheral microcirculation in diabetic patients often leads to severe complications in the lower extremities, such as foot infections and ulcerations. In this study, a novel aescin-based formulation has been evaluated as a potential approach to prevent skin breaks and ulcerations by improving the peripheral microcirculation and skin hydration. PATIENTS AND METHODS: In this registry study, 63 patients with moderate diabetic microangiopathy were recruited. Informed participants freely decided to follow either a standard management (SM) to prevent diabetic foot diseases (n = 31) or SM associated with topical application of the aescin-based cream (n = 32). Peripheral microcirculatory parameters such as resting skin flux, venoarteriolar response and transcutaneous gas tension were evaluated at inclusion and after 8 weeks. In addition, several skin parameters of the foot area, such as integrity (as number of skin breaks/patients), hydration and content of dead cells were assessed at the defined observational study periods. RESULTS: Improvements in cutaneous peripheral microcirculation parameters were observed at 8 weeks in both groups; however, a remarkable and significant beneficial effect resulted to be exerted by the aescin-based cream treatment. In fact, the microcirculatory parameters evaluated significantly improved in the standard management + aescin-based cream group, compared with baseline and with the standard management group. Similar findings were reported for skin parameters of the foot area. CONCLUSIONS: The topical formulation containing aescin could represent a valid approach to manage skin wounds and prevent skin ulcerations in patients affected by moderate diabetic microangiopathy.
[Mh] Termos MeSH primário: Angiopatias Diabéticas/tratamento farmacológico
Escina/uso terapêutico
[Mh] Termos MeSH secundário: Administração Cutânea
Pé Diabético
Feminino

Seres Humanos
Masculino
Microcirculação
Meia-Idade
Sistema de Registros
Pele
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
6805-41-0 (Escin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161111
[St] Status:MEDLINE


  7 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27727329
[Au] Autor:Domanski D; Zegrocka-Stendel O; Perzanowska A; Dutkiewicz M; Kowalewska M; Grabowska I; Maciejko D; Fogtman A; Dadlez M; Koziak K
[Ad] Endereço:Laboratory of Mass Spectrometry, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
[Ti] Título:Molecular Mechanism for Cellular Response to ß-Escin and Its Therapeutic Implications.
[So] Source:PLoS One;11(10):e0164365, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ß-escin is a mixture of triterpene saponins isolated from the horse chestnut seeds (Aesculus hippocastanum L.). The anti-edematous, anti-inflammatory and venotonic properties of ß-escin have been the most extensively clinically investigated effects of this plant-based drug and randomized controlled trials have proved the efficacy of ß-escin for the treatment of chronic venous insufficiency. However, despite the clinical recognition of the drug its pharmacological mechanism of action still remains largely elusive. To determine the cellular and molecular basis for the therapeutic effectiveness of ß-escin we performed discovery and targeted proteomic analyses and in vitro evaluation of cellular and molecular responses in human endothelial cells under inflammatory conditions. Our results demonstrate that in endothelial cells ß-escin potently induces cholesterol synthesis which is rapidly followed with marked fall in actin cytoskeleton integrity. The concomitant changes in cell functioning result in a significantly diminished responses to TNF-α stimulation. These include reduced migration, alleviated endothelial monolayer permeability, and inhibition of NFκB signal transduction leading to down-expression of TNF-α-induced effector proteins. Moreover, the study provides evidence for novel therapeutic potential of ß-escin beyond the current vascular indications.
[Mh] Termos MeSH primário: Aesculus/química
Proliferação Celular/efeitos dos fármacos
Escina/farmacologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/efeitos dos fármacos
Citoesqueleto de Actina/metabolismo
Aesculus/metabolismo
Movimento Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Colesterol/biossíntese
Escina/química
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
NF-kappa B/metabolismo
Permeabilidade/efeitos dos fármacos
Proteoma/análise
Proteoma/efeitos dos fármacos
Proteômica
Sementes/química
Sementes/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Proteome); 0 (Tumor Necrosis Factor-alpha); 6805-41-0 (Escin); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161012
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164365


  8 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26952957
[Au] Autor:Yao DF; Mills JN
[Ti] Título:Male infertility: lifestyle factors and holistic, complementary, and alternative therapies.
[So] Source:Asian J Androl;18(3):410-8, 2016 May-Jun.
[Is] ISSN:1745-7262
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:While we may be comfortable with an allopathic approach to male infertility, we are also responsible for knowledge about lifestyle modifications and holistic, complementary, and alternative therapies that are used by many of our patients. This paper provides an evidence-based review separating fact from fiction for several of these therapies. There is sufficient literature to support weight reduction by diet and exercise, smoking cessation, and alcohol moderation. Supplements that have demonstrated positive effects on male fertility on small randomized controlled trial (RCT) include aescin, coenzyme Q 10 , glutathione, Korean red ginseng, L-carnitine, nigella sativa, omega-3, selenium, a combination of zinc and folate, and the Menevit antioxidant. There is no support for the use of Vitamin C, Vitamin E, or saffron. The data for Chinese herbal medications, acupuncture, mind-body practice, scrotal cooling, and faith-based healing are sparse or inconclusive.
[Mh] Termos MeSH primário: Terapias Complementares
Suplementos Nutricionais
Infertilidade Masculina/terapia
Obesidade/terapia
[Mh] Termos MeSH secundário: Terapia por Acupuntura
Antioxidantes/uso terapêutico
Carnitina/uso terapêutico
Crioterapia
Medicamentos de Ervas Chinesas/uso terapêutico
Escina/uso terapêutico
Cura pela Fé
Ácidos Graxos Ômega-3/uso terapêutico
Glutationa/uso terapêutico
Seres Humanos
Estilo de Vida
Masculino
Medicina Tradicional Chinesa
Micronutrientes/uso terapêutico
Nigella sativa
Panax
Selênio/uso terapêutico
Ubiquinona/uso terapêutico
Zinco/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (Drugs, Chinese Herbal); 0 (Fatty Acids, Omega-3); 0 (Micronutrients); 1339-63-5 (Ubiquinone); 6805-41-0 (Escin); GAN16C9B8O (Glutathione); H6241UJ22B (Selenium); J41CSQ7QDS (Zinc); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160309
[St] Status:MEDLINE
[do] DOI:10.4103/1008-682X.175779


  9 / 447 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26824290
[Au] Autor:Mojzisová G; Kello M; Pilátová M; Tomecková V; Vasková J; Vasko L; Bernátová S; Mirossay L; Mojzis J
[Ad] Endereço:Department of Experimental Medicine, Faculty of Medicine, P. J. Safárik University, 040 11 Kosice, Slovak Republic.
[Ti] Título:Antiproliferative effect of ß-escin - an in vitro study.
[So] Source:Acta Biochim Pol;63(1):79-87, 2016.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study examined the antiproliferative effects of ß-escin (E) in cancer cells. The study showed that E inhibited cancer cells growth in a dose-dependent manner. The flow cytometric analysis revealed an escin-induced increase in the sub-G1 DNA content, which is considered to be a marker of apoptosis. Apoptosis was also confirmed by annexin V staining and DNA fragmentation assay. These effects were associated with increased generation of reactive oxygen species (ROS), caspase-3 activation and decreased mitochondrial membrane potential (MMP). Moreover, escin decreased mitochondrial protein content and mitochondrial fluorescence intensity as well as caused depletion of glutathione (GSH). However, activity of glutathione peroxidase (GPx) and glutathione reductase (GR) was not significantly changed in escin-treated cells. In conclusion, our results demonstrated that E has apoptotic effects in human cancer cells through the mechanisms involving mitochondrial perturbation. Although the exact mechanism needs to be investigated further, it can be concluded that E may be a useful candidate agent for cancer treatment.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Escina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Linhagem Celular Tumoral
Fragmentação do DNA
Relação Dose-Resposta a Droga
Ativação Enzimática
Glutationa/metabolismo
Glutationa Peroxidase/metabolismo
Glutationa Redutase/metabolismo
Seres Humanos
Técnicas In Vitro
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Neoplasias/enzimologia
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 6805-41-0 (Escin); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.8.1.7 (Glutathione Reductase); EC 3.4.22.- (Caspase 3); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160130
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2015_1013


  10 / 447 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26773773
[Au] Autor:Du Y; Song Y; Zhang L; Zhang M; Fu F
[Ad] Endereço:Key Laboratory of Molecular Pharmacology and Drug Evaluation (Ministry of Education of China), School of Pharmacy, Yantai University, Yantai 264005, PR China.
[Ti] Título:Combined treatment with low dose prednisone and escin improves the anti-arthritic effect in experimental arthritis.
[So] Source:Int Immunopharmacol;31:257-65, 2016 Feb.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study was aimed at investigating whether low dose oral prednisone combined with escin could inhibit the progression of adjuvant-induced arthritis (AIA) in rats. Adjuvant arthritis was induced in SD rats began day 1 for 28 days. Prednisone at doses of 2, 10 mg/kg/day alone or escin at doses of 5, 10 mg/kg/day alone, or prednisone at dose of 2 mg/kg/day with escin at doses of 5 or 10 mg/kg/day were given to different groups of rats intragastrically from day 13 to 28 respectively. Paw swelling, arthritic index, histological and radiographic changes were assessed to evaluate the anti-arthritic effect. Weight growth, spleen and thymus indexes were also calculated. Serum samples were collected for estimation of pro-inflammatory cytokines. Rats developed erosive arthritis of the hind paw when immunized with adjuvant. Prednisone 2 mg/kg combined with escin 5 or 10 mg/kg significantly inhibited the paw swelling. Histopathological and radiographic analysis showed a marked decrease of synovial inflammatory infiltration, synovial hyperplasia and bone erosion by combination therapy, which also markedly suppressed the expression of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6). No significant changes were found in monotherapy group except prednisone 10 mg/kg group. Furthermore, combined treatment rescued some of GCs' adverse effects evidenced by increase in body weight and decrease in index of spleen compared with untreated AIA rats. In conclusion, the combination therapy possessed synergistic anti-arthritic efficacy and reduced adverse effect, which may play a role in the management of human RA.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Artrite Experimental/tratamento farmacológico
Escina/administração & dosagem
Prednisona/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/uso terapêutico
Sinergismo Farmacológico
Quimioterapia Combinada
Escina/uso terapêutico
Seres Humanos
Mediadores da Inflamação/metabolismo
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Masculino
Prednisona/uso terapêutico
Ratos
Ratos Sprague-Dawley
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 6805-41-0 (Escin); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160117
[St] Status:MEDLINE



página 1 de 45 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde