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[PMID]:29191011
[Au] Autor:Zhang Z; Wang H; Wang K; Jiang L; Wang D
[Ti] Título:Use of Lentinan To Control Sharp Eyespot of Wheat, and the Mechanism Involved.
[So] Source:J Agric Food Chem;65(50):10891-10898, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lentinan (LNT), a complex polysaccharide with a ß-(1→3)-linked backbone of d-glucose residues, has been reported to inhibit plant diseases. Our objective was to explore the efficacy and action mechanism of LNT used as a seed dressing to control sharp eyespot of wheat. Seed dressing promoted wheat growth. At control germination rates of 50%, 8 g of LNT/100 kg of seeds of the Jimai 22, Shannong 23, and Luyuan 502 cultivars significantly increased seed germination to 54%, 52%, and 51%, respectively. Seven days after emergence, the heights and root activity of wheat treated with LNT were significantly greater than those of controls. These effects were dose-dependent. At this time, the plant heights of Jimai 22, Shannong 23, and Luyuan 502 cultivars were 9.52, 8.52, and 10.52 cm, respectively, significantly higher than that of the controls. LNT prevented the development of wheat sharp eyespot. In the highly susceptible Jimai 22 cultivar, sharp eyespot development was reduced by 33.7%, 31.9%, and 30.4% at 7, 14, and 21 days after germination. LNT somewhat increased phenylalanine ammonia-lyase, peroxidase, and superoxide dismutase activity; reduced the malondialdehyde content; increased chlorophyll a and b levels; and enhanced the root vigor of wheat. These effects peaked 7 days after germination. LNT increased transcription of the genes encoding alternative oxidase (AOX) and ß-1,3-glucanase (GLU), the salicylic acid signaling pathway-related gene NbPR1a, and the sharp eyespot resistance-related gene RS33. A significant dose-effect relationship was evident in terms of AOX transcription; we thus speculate that AOX may be the target gene.
[Mh] Termos MeSH primário: Fungicidas Industriais/farmacologia
Lentinano/farmacologia
Doenças das Plantas/prevenção & controle
Extratos Vegetais/farmacologia
Rhizoctonia/efeitos dos fármacos
Cogumelos Shiitake/química
Triticum/microbiologia
[Mh] Termos MeSH secundário: Clorofila/metabolismo
Fungicidas Industriais/química
Germinação/efeitos dos fármacos
Lentinano/química
Malondialdeído/metabolismo
Fenilalanina Amônia-Liase/genética
Fenilalanina Amônia-Liase/metabolismo
Doenças das Plantas/microbiologia
Extratos Vegetais/química
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Rhizoctonia/fisiologia
Sementes/crescimento & desenvolvimento
Sementes/microbiologia
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Triticum/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungicides, Industrial); 0 (Plant Extracts); 0 (Plant Proteins); 1406-65-1 (Chlorophyll); 37339-90-5 (Lentinan); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); EC 4.3.1.24 (Phenylalanine Ammonia-Lyase); YF5Q9EJC8Y (chlorophyll a)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04665


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[PMID]:28364801
[Au] Autor:Wang J; Wang Y; Shen L; Qian Y; Yang J; Wang F
[Ad] Endereço:Tobacco Research Institute, Chinese Academy of Agricultural Sciences, 11 Keyuanjing Si Rd., Laoshan District, Qingdao, China.
[Ti] Título:Sulfated lentinan induced mitochondrial dysfunction leads to programmed cell death of tobacco BY-2 cells.
[So] Source:Pestic Biochem Physiol;137:27-35, 2017 Apr.
[Is] ISSN:1095-9939
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sulphated lentinan (sLTN) is known to act as a resistance inducer by causing programmed cell death (PCD) in tobacco suspension cells. However, the underlying mechanism of this effect is largely unknown. Using tobacco BY-2 cell model, morphological and biochemical studies revealed that mitochondrial reactive oxygen species (ROS) production and mitochondrial dysfunction contribute to sLNT induced PCD. Cell viability, and HO/PI fluorescence imaging and TUNEL assays confirmed a typical cell death process caused by sLNT. Acetylsalicylic acid (an ROS scavenger), diphenylene iodonium (an inhibitor of NADPH oxidases) and protonophore carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (a protonophore and an uncoupler of mitochondrial oxidative phosphorylation) inhibited sLNT-induced H O generation and cell death, suggesting that ROS generation linked, at least partly, to a mitochondrial dysfunction and caspase-like activation. This conclusion was further confirmed by double-stained cells with the mitochondria-specific marker MitoTracker RedCMXRos and the ROS probe H DCFDA. Moreover, the sLNT-induced PCD of BY-2 cells required cellular metabolism as up-regulation of the AOX family gene transcripts and induction of the SA biosynthesis, the TCA cycle, and miETC related genes were observed. It is concluded that mitochondria play an essential role in the signaling pathway of sLNT-induced ROS generation, which possibly provided new insight into the sLNT-mediated antiviral response, including PCD.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Lentinano/análogos & derivados
Mitocôndrias/efeitos dos fármacos
Tabaco/efeitos dos fármacos
[Mh] Termos MeSH secundário: Caspase 3/metabolismo
Caspase 9/metabolismo
Linhagem Celular
Citocromos c/metabolismo
Expressão Gênica/efeitos dos fármacos
Complexo Cetoglutarato Desidrogenase/genética
Lentinano/toxicidade
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/fisiologia
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Tabaco/citologia
Tabaco/genética
Tabaco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (Reactive Oxygen Species); 0 (mitochondrial permeability transition pore); 114285-68-6 (lentinan sulfate); 37339-90-5 (Lentinan); 9007-43-6 (Cytochromes c); EC 1.2.4.2 (Ketoglutarate Dehydrogenase Complex); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE


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[PMID]:27566177
[Au] Autor:Stephany MP; Chung S; Handler MZ; Handler NS; Handler GA; Schwartz RA
[Ad] Endereço:University of Nebraska Medical Center, College of Medicine, Omaha, NE, USA.
[Ti] Título:Shiitake Mushroom Dermatitis: A Review.
[So] Source:Am J Clin Dermatol;17(5):485-489, 2016 Oct.
[Is] ISSN:1179-1888
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Shiitake mushroom dermatitis is a cutaneous reaction caused by the consumption of raw or undercooked shiitake mushrooms. Symptoms include linear erythematous eruptions with papules, papulovesicles or plaques, and severe pruritus. It is likely caused by lentinan, a heat-inactivated beta-glucan polysaccharide. Cases were initially reported in Japan but have now been documented in other Asian countries, North America, South America, and Europe, as this mushroom is now cultivated and consumed worldwide. Shiitake mushroom dermatitis may result from mushroom ingestion or from handling, which can result in an allergic contact dermatitis.
[Mh] Termos MeSH primário: Dermatite/etiologia
Hipersensibilidade Alimentar/etiologia
Cogumelos Shiitake/química
[Mh] Termos MeSH secundário: Culinária
Dermatite/patologia
Dermatite Alérgica de Contato/etiologia
Dermatite Alérgica de Contato/patologia
Hipersensibilidade Alimentar/patologia
Seres Humanos
Lentinano/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
37339-90-5 (Lentinan)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170130
[Lr] Data última revisão:
170130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE


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[PMID]:27501505
[Au] Autor:Yoshino S; Nishikawa K; Morita S; Takahashi T; Sakata K; Nagao J; Nemoto H; Murakami N; Matsuda T; Hasegawa H; Shimizu R; Yoshikawa T; Osanai H; Imano M; Naitoh H; Tanaka A; Tajiri T; Gochi A; Suzuki M; Sakamoto J; Saji S; Oka M
[Ad] Endereço:Department of Digestive Surgery and Surgical Oncology, Yamaguchi University Graduate School of Medicine, Ube, Japan. Electronic address: sigefumi@yamaguchi-u.ac.jp.
[Ti] Título:Randomised phase III study of S-1 alone versus S-1 plus lentinan for unresectable or recurrent gastric cancer (JFMC36-0701).
[So] Source:Eur J Cancer;65:164-71, 2016 Sep.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lentinan (LNT) is a purified ß-1, 3-glucan that augments immune responses. The present study was conducted to assess the efficacy of LNT in combination with S-1 as a first-line treatment for unresectable or recurrent gastric cancer. PATIENTS AND METHODS: Eligible patients were randomly assigned to receive S-1 alone or S-1 plus LNT. The primary end-point was overall survival (OS). Secondary end-points were time-to-treatment failure (TTF), overall response rate (ORR), safety, quality of life (QOL), and biomarker. The percentages of LNT-binding monocytes in peripheral blood prior to treatment were analysed for the biomarker assessment. RESULTS: One hundred and fifty-four and 155 patients were randomly assigned to receive S-1 alone or S-1 plus LNT, respectively. The median OS was 13.8 and 9.9 months (P = 0.208), the median TTF was 4.3 and 2.6 months (P < 0.001), the ORR was 22.3% and 18.7% for the S-1 and S-1 plus LNT groups, respectively. The incidences of haematologic and non-haematologic adverse events were similar, and no significant changes in QOL scores were observed during the treatment in both groups. In a subpopulation of patients with LNT-binding monocytes ≥2%, patients who received more than two cycles of chemotherapy showed a longer survival time in the S-1 plus LNT group. CONCLUSIONS: OS did not improve and TTF was significantly worse in the S-1 plus LNT group as compared with the S-1-only group. This study showed no efficacy of LNT when combined with S-1 treatment in patients with unresectable or recurrent gastric cancer. CLINICAL TRIAL REGISTRATION ID NUMBER: UMIN 000000574.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Lentinano/uso terapêutico
Ácido Oxônico/uso terapêutico
Neoplasias Gástricas/tratamento farmacológico
Tegafur/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/análise
Combinação de Medicamentos
Feminino
Seres Humanos
Masculino
Meia-Idade
Monócitos/metabolismo
Qualidade de Vida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Drug Combinations); 150863-82-4 (S 1 (combination)); 1548R74NSZ (Tegafur); 37339-90-5 (Lentinan); 5VT6420TIG (Oxonic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160809
[St] Status:MEDLINE


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[PMID]:27444655
[Au] Autor:Zhang Y; Mei H; Shan W; Shi L; Chang X; Zhu Y; Chen F; Han X
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
[Ti] Título:Lentinan protects pancreatic ß cells from STZ-induced damage.
[So] Source:J Cell Mol Med;20(10):1803-12, 2016 Oct.
[Is] ISSN:1582-4934
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pancreatic ß-cell death or dysfunction mediated by oxidative stress underlies the development and progression of diabetes mellitus (DM). In this study, we evaluated the effect of lentinan (LNT), an active ingredient purified from the bodies of Lentinus edodes, on pancreatic ß-cell apoptosis and dysfunction caused by streptozotocin (STZ) and the possible mechanisms implicated. The rat insulinoma cell line INS-1 were pre-treated with the indicated concentration of LNT for 30 min. and then incubated for 24 hrs with or without 0.5 mM STZ. We found that STZ treatment causes apoptosis of INS-1 cells by enhancement of intracellular reactive oxygen species (ROS) accumulation, inducible nitric oxide synthase (iNOS) expression and nitric oxide release and activation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways. However, LNT significantly increased cell viability and effectively attenuated STZ-induced ROS production, iNOS expression and nitric oxide release and the activation of JNK and p38 MAPK in a dose-dependent manner in vitro. Moreover, LNT dose-dependently prevented STZ-induced inhibition of insulin synthesis by blocking the activation of nuclear factor kappa beta and increasing the level of Pdx-1 in INS-1 cells. Together these findings suggest that LNT could protect against pancreatic ß-cell apoptosis and dysfunction caused by STZ and therefore may be a potential pharmacological agent for preventing pancreatic ß-cell damage caused by oxidative stress associated with diabetes.
[Mh] Termos MeSH primário: Citoproteção/efeitos dos fármacos
Células Secretoras de Insulina/patologia
Lentinano/farmacologia
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Ativação Enzimática/efeitos dos fármacos
Proteínas de Homeodomínio/metabolismo
Insulina/biossíntese
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Ratos
Espécies Reativas de Oxigênio/metabolismo
Estreptozocina
Transativadores/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Insulin); 0 (NF-kappa B); 0 (Protective Agents); 0 (Reactive Oxygen Species); 0 (Trans-Activators); 0 (pancreatic and duodenal homeobox 1 protein); 31C4KY9ESH (Nitric Oxide); 37339-90-5 (Lentinan); 5W494URQ81 (Streptozocin); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160723
[St] Status:MEDLINE
[do] DOI:10.1111/jcmm.12865


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[PMID]:27387601
[Au] Autor:Shivahare R; Ali W; Singh US; Natu SM; Khattri S; Puri SK; Gupta S
[Ad] Endereço:Department of Pathology, King George's Medical University, Lucknow, India. rahul_biotech08@yahoo.com.
[Ti] Título:Immunoprotective effect of lentinan in combination with miltefosine on Leishmania-infected J-774A.1 macrophages.
[So] Source:Parasite Immunol;38(10):618-27, 2016 Oct.
[Is] ISSN:1365-3024
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rejuvenation of deteriorated host immune functions is imperative for successful annihilation of Leishmania parasites. The use of immunomodulatory agents may have several advantages as they conquer immunosuppression and, when given in combination, improve current therapeutic regimens. We herein investigated the immunostimulatory potency of a ß-glucan, lentinan either alone or in combination with short dose of standard drug, miltefosine on Leishmania-infected J-774A.1 macrophages. Our study shows that infected macrophages when stimulated with 2.5 µg/mL and above concentrations of lentinan secreted significant amount of host-protective molecules. The in vitro interaction between lentinan and miltefosine showed some synergy (mean sum of fractional inhibitory concentration [mean ∑FIC] 0.87) at IC50 level. Lentinan (2.5 µg/mL) plus low-dose miltefosine (2 µM) displayed heightened level of pro-inflammatory cytokines, IL-12 (13.6-fold) and TNF-α (6.8-fold) along with nitric oxide (7.2-fold higher) when compared with infected control. In combination group, we also observed remarkably (P<.001) suppressed levels of anti-inflammatory cytokines, IL-10 and TGF-ß, than that of untreated macrophages. Additionally, in comparison with infected group, we observed significant induction in phagocytic activity of macrophages in combination with treated group. Collectively, these findings emphasize the immunostimulatory effect of lentinan alone and in combination with low dose of miltefosine against Leishmania donovani.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Antiprotozoários/farmacologia
Leishmania donovani/imunologia
Lentinano/farmacologia
Macrófagos/efeitos dos fármacos
Fosforilcolina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Citocinas/metabolismo
Fatores Imunológicos/farmacologia
Leishmania donovani/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/parasitologia
Camundongos
Óxido Nítrico/metabolismo
Fosforilcolina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antiprotozoal Agents); 0 (Cytokines); 0 (Immunologic Factors); 107-73-3 (Phosphorylcholine); 31C4KY9ESH (Nitric Oxide); 37339-90-5 (Lentinan); 53EY29W7EC (miltefosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160709
[St] Status:MEDLINE
[do] DOI:10.1111/pim.12346


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[PMID]:27156806
[Au] Autor:Wang SX; Liu QY; Li Y
[Ad] Endereço:Department of General Surgery, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China; Department of General Surgery, First Hospital of Handan, Hebei Province 056000, PR China.
[Ti] Título:Lentinan ameliorates burn sepsis by attenuating CD4 CD25 Tregs.
[So] Source:Burns;42(7):1513-1521, 2016 Nov.
[Is] ISSN:1879-1409
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: The aim of our study was to investigate the effect of lentinan on regulatory T cells (Tregs) in sepsis, especially on the generation of interleukin (IL)-10 via regulation of Erk-FoxO1 signaling. METHODS: BalB/c mice were randomized into five groups: sham group, the group with burns plus Pseudomonas aeruginosa infection, and the groups with burns plus P. aeruginosa infection administered 40, 100, and 250mg/kg of lentinan. The mice were sacrificed on postburn days 0, 1, 2, 3, and 4, respectively, with eight animals per group at each time point. The peripheral blood CD4 CD25 Tregs and CD4 T cells were isolated using magnetic microbeads. The phenotypes were analyzed by flow cytometry. The cytokine levels were determined with enzyme-linked immunosorbent assay (ELISA). Signal transduction was studied by Western blot, quantitative polymerase chain reaction (qPCR), and luciferase assay. RESULTS: The IL-10-producing capacity of CD4 CD25 Tregs was significantly enhanced in the group with burns plus P. aeruginosa infection, compared with the sham group. Administration of lentinan significantly decreased IL-10 production and FoxP3 expression of CD4 CD25 Tregs. The proliferative activities of CD4 T cells, however, were restored. Lentinan decreased lipopolysaccharide (LPS)-induced IL-10 production in the Tregs isolated from burned mice. In addition, lentinan attenuated LPS-stimulated Erk-FoxO1 activation. CONCLUSIONS: Lentinan may improve the outcome of postburn sepsis by suppressing LPS-triggered Erk-FoxO1 activation. Consequently, the hyperfunction of CD4 CD25 Tregs is inhibited, leading to a shift in the inflammatory status from Th2 to Th1 in postburn sepsis.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Queimaduras/imunologia
Lentinano/farmacologia
Infecções por Pseudomonas/imunologia
Sepse/imunologia
Linfócitos T Reguladores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Proliferação Celular/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Proteína Forkhead Box O1/efeitos dos fármacos
Proteína Forkhead Box O1/genética
Proteína Forkhead Box O1/imunologia
Interleucina-10/genética
Interleucina-10/imunologia
Subunidade alfa de Receptor de Interleucina-2/imunologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/genética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Pseudomonas aeruginosa
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (IL10 protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 130068-27-8 (Interleukin-10); 37339-90-5 (Lentinan)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160510
[St] Status:MEDLINE


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[PMID]:27130669
[Au] Autor:Zhang Y; Li Q; Wang J; Cheng F; Huang X; Cheng Y; Wang K
[Ad] Endereço:Department of Pharmacy, Union Hospital of Huazhong University of Science and Technology, No. 1227, Jiefang Road, 430030 Wuhan, China.
[Ti] Título:Polysaccharide from Lentinus edodes combined with oxaliplatin possesses the synergy and attenuation effect in hepatocellular carcinoma.
[So] Source:Cancer Lett;377(2):117-25, 2016 07 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Despite the great progress in the treatment of hepatocellular carcinoma, combination chemotherapy is still the main choice of treatment for patients with unresectable metastatic or recurrent hepatocellular cancer. Lentinan, which has been used as an immunomodulator in the treatment of cancer, possesses anti-tumor activities. However, the mechanisms by which Lentinan inhibits hepatocellular carcinoma remain unknown. Our study showed that Lentinan has a significantly synergistic anti-tumor effect with oxaliplatin against HepG2 cells in vitro and in H22 tumor-bearing mice through the mitochondria pathway and for the inhibition of NF-κB, Stat3 and survivin signaling. Moreover, Lentinan moderated side effects induced by oxaliplatin. These findings suggested that Lentinan may be an ideal agent for the combination therapy of oxaliplatin against hepatocellular carcinoma.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma Hepatocelular/tratamento farmacológico
Lentinano/farmacologia
Neoplasias Hepáticas/tratamento farmacológico
Compostos Organoplatínicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/toxicidade
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Células Hep G2
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Proteínas Inibidoras de Apoptose/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Masculino
Camundongos Endogâmicos BALB C
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
NF-kappa B/metabolismo
Compostos Organoplatínicos/toxicidade
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transfecção
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Birc5 protein, mouse); 0 (Inhibitor of Apoptosis Proteins); 0 (NF-kappa B); 0 (Organoplatinum Compounds); 0 (Repressor Proteins); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 04ZR38536J (oxaliplatin); 37339-90-5 (Lentinan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160501
[St] Status:MEDLINE


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[PMID]:27121155
[Au] Autor:Liu Q; Dong L; Li H; Yuan J; Peng Y; Dai S
[Ad] Endereço:Department of Radiology, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
[Ti] Título:Lentinan mitigates therarubicin-induced myelosuppression by activating bone marrow-derived macrophages in an MAPK/NF-κB-dependent manner.
[So] Source:Oncol Rep;36(1):315-23, 2016 Jul.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Bone marrow (BM) suppression (also known as myelosuppression) is the most common and most severe side-effect of therarubicin (THP) and thereby limits the clinical application of this anticancer agent. Lentinan (LNT), a glucan extracted from dried shiitake mushrooms (Lentinula edodes), exhibits a variety of pharmacological activities. The objectives of the present study were to determine the effect of LNT on the myelosuppression of THP-treated mice and to examine the pharmacological mechanism of these effects. In vivo experiments indicated that non-cytotoxic levels of LNT strongly increased blood myeloperoxidase (MPO) activity; improved BM structural injuries; increased the numbers of leukocytes and neutrophils in the blood and BM; elevated the blood levels of granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF); and reduced the self-healing period in THP-treated mice. In vitro experiments indicated that LNT increased the viability of BM-derived macrophages (BMDMs) in a time- and dose-dependent manner without toxic side-effects and markedly increased the release of G-CSF, GM-CSF and M-CSF by BMDMs. Further analyses revealed that LNT activated the NF-κB and MAPK signalling pathways and promoted the nuclear import of p65 and that BAY 11-7082 (a specific inhibitor of NF-κB) suppressed the release of G-CSF, GM-CSF and M-CSF. Furthermore, we found that U0126, SB203580 and SP600125 (specific inhibitors of ERK, p38 and JNK, respectively) markedly inhibited the IKK/IκB/NF-κB-dependent release of G-CSF, GM-CSF and M-CSF. In conclusion, LNT induces the production of G-CSF, GM-CSF and M-CSF by activating the MAPK/NF-κB signalling pathway in BM cells, thereby mitigating THP-induced myelosuppression.
[Mh] Termos MeSH primário: Medula Óssea/efeitos dos fármacos
Doxorrubicina/análogos & derivados
Lentinano/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
[Mh] Termos MeSH secundário: Animais
Antracenos/farmacologia
Medula Óssea/metabolismo
Doxorrubicina/farmacologia
Feminino
Fator Estimulador de Colônias de Granulócitos/metabolismo
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Proteínas I-kappa B/metabolismo
Imidazóis/farmacologia
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Macrófagos/metabolismo
Masculino
Camundongos
Neutrófilos/efeitos dos fármacos
Neutrófilos/metabolismo
Piridinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (I-kappa B Proteins); 0 (Imidazoles); 0 (NF-kappa B); 0 (Pyridines); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 1TW30Y2766 (pyrazolanthrone); 37339-90-5 (Lentinan); 80168379AG (Doxorubicin); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); D58G680W0G (pirarubicin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160429
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.4769


  10 / 395 MEDLINE  
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[PMID]:27093515
[Au] Autor:Chen Q; Peng H; Dong L; Chen L; Ma X; Peng Y; Dai S; Liu Q
[Ad] Endereço:Department of Obstetrics and Gynecology, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:Activation of the NRF2-ARE signalling pathway by the Lentinula edodes polysaccharose LNT alleviates ROS-mediated cisplatin nephrotoxicity.
[So] Source:Int Immunopharmacol;36:1-8, 2016 Jul.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The nephrotoxicity of cisplatin (cis-DDP) limits its general clinical applications. Lentinan (LNT), a dextran extracted from the mushroom Lentinula edodes, has been shown to have multiple pharmacological activities. The primary objective of the current study was to determine whether and how LNT alleviates cis-DDP- induced cytotoxicity in HK-2 cells and nephrotoxicity in mice. LNT did not interfere with cisplatin's anti-tumour efficacy in vitro and functioned cooperatively with cis-DDP to inhibit activity in HeLa and A549 tumour cells. LNT alleviated the cis-DDP-induced decrease in HK-2 cell viability, caspase-3 activation and cleavage of the DNA repair enzyme PARP, decreased HK-2 cell apoptosis and inhibited reactive oxygen species (ROS) accumulation in HK-2 cells. The inhibitor of ROS (N-acetyl-L-cysteine, NAC) could decreased the apoptosis of HK-2 cell. In addition, LNT significantly prevented cis-DDP-induced kidney injury in vivo. LNT itself could not eliminate ROS levels in vitro. Further studies demonstrated that LNT induced NF-E2 p45-related factor 2 (Nrf2) protein and mRNA expression in a time- and dose-dependent manner. LNT promoted Nrf2 translocation to the nucleus and binding to the antioxidant-response element (ARE) sequence and induced the transcription and translation of heme oxygenase 1 (HO-1), aldo-keto reductases 1C1 and 1C2 (AKR1C), and NADP(H):quinone oxidoreductase 1 (NQO1). Finally, we used hNrf2 siRNA and an Nrf2 agonist (tBHQ) to inhibit or enhance Nrf2 expression. The results demonstrated that the LNT-mediated alleviation of cis-DDP-induced nephrotoxicity was achieved by preventing the accumulation of ROS in a manner that depended on the activation of the Nrf2-ARE signalling pathway.
[Mh] Termos MeSH primário: Hidrolases de Éster Carboxílico/metabolismo
Cisplatino/uso terapêutico
Tratamento Farmacológico
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/prevenção & controle
Rim/efeitos dos fármacos
Lentinano/uso terapêutico
Fator 2 Relacionado a NF-E2/metabolismo
Cogumelos Shiitake
[Mh] Termos MeSH secundário: Células A549
Animais
Apoptose/efeitos dos fármacos
Hidrolases de Éster Carboxílico/genética
Sobrevivência Celular/efeitos dos fármacos
Feminino
Células HeLa
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Rim/patologia
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/genética
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Reactive Oxygen Species); 37339-90-5 (Lentinan); BBX060AN9V (Hydrogen Peroxide); EC 3.1.1.- (Carboxylic Ester Hydrolases); EC 3.1.1.2 (arylesterase); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170805
[Lr] Data última revisão:
170805
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160420
[St] Status:MEDLINE



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