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Pesquisa : B01.650.940.800.575.912.250.401.012 [Categoria DeCS]
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[PMID]:28682903
[Au] Autor:Huang J; Zhang W; Li X; Feng S; Ye G; Wei H; Gong X
[Ad] Endereço:aDepartment of Gastroenterology bDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
[Ti] Título:Acute abrin poisoning treated with continuous renal replacement therapy and hemoperfusion successfully: A case report.
[So] Source:Medicine (Baltimore);96(27):e7423, 2017 Jul.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Abrin is a highly toxic protein obtained from the seeds of Abrus precatorius, but poisoning due to ingestion of A precatorius is extremely rare in China. PATIENT CONCERNS: A 16-year-old girl, perfectly healthy before, was admitted to the department of gastroenterology owing to intentional ingestion of 10 crushed A precatorius seeds, with multiple episodes of somnolent and anxious mental status, vomiting, abdominal pain, diarrhea, hematochezia, and hematuria. DIAGNOSIS: Acute abrin poisoning. INTERVENTIONS: We immediately took effective measures including gastric lavage, purgation, gastric acid suppression by proton pump inhibitor (PPI), liver protection, hemostasis, blood volume and electrolytes resuscitation, continuous renal replacement therapy (CRRT), and hemoperfusion (HP). OUTCOMES: Her unwell mental status was improved to the point at which she became conscious and relaxed. The symptoms of vomiting, abdominal pain, diarrhea, hematochezia, and hematuria disappeared gradually. The girl eventually made an excellent recovery with no complications at her 3-month follow-up. LESSONS: The combination of CRRT and HP is an efficient measure in the treatment of abrin poisoning for which there is no specific antidote. This is the first reported case of an abrin poisoning patient successfully treated by CRRT plus HP. Our experience will be useful to other physicians in managing patients of acute abrin poisoning in the future.
[Mh] Termos MeSH primário: Abrina/envenenamento
Abrus/envenenamento
Hemoperfusão
Terapia de Substituição Renal
[Mh] Termos MeSH secundário: Adolescente
Feminino
Seres Humanos
Intenção
Sementes/envenenamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
1393-62-0 (Abrin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007423


  2 / 93 MEDLINE  
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[PMID]:28543759
[Au] Autor:Sinha N; Panda PK; Naik PP; Das DN; Mukhopadhyay S; Maiti TK; Shanmugam MK; Chinnathambi A; Zayed ME; Alharbi SA; Sethi G; Agarwal R; Bhutia SK
[Ad] Endereço:Department of Life Science, National Institute of Technology, Rourkela, India.
[Ti] Título:Abrus agglutinin promotes irreparable DNA damage by triggering ROS generation followed by ATM-p73 mediated apoptosis in oral squamous cell carcinoma.
[So] Source:Mol Carcinog;56(11):2400-2413, 2017 Nov.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oral cancer, a type of head and neck cancer, is ranked as one of the top most malignancies in India. Herein, we evaluated the anticancer efficacy of Abrus agglutinin (AGG), a plant lectin, in oral squamous cell carcinoma. AGG selectively inhibited cell growth, and caused cell cycle arrest and mitochondrial apoptosis through a reactive oxygen species (ROS)-mediated ATM-p73 dependent pathway in FaDu cells. AGG-induced ROS accumulation was identified as the major mechanism regulating apoptosis, DNA damage and DNA-damage response, which were significantly reversed by ROS scavenger N-acetylcysteine (NAC). Moreover, AGG was found to interact with mitochondrial manganese-dependent superoxide dismutase that might inhibit its activity and increase ROS in FaDu cells. In oral cancer p53 is mutated, thus we focused on p73; AGG resulted in p73 upregulation and knock down of p73 caused a decrease in AGG-induced apoptosis. Interestingly, AGG-dependent p73 expression was found to be regulated by ROS, which was reversed by NAC treatment. A reduction in the level of p73 in AGG-treated shATM cells was found to be associated with a decreased apoptosis. Moreover, administration of AGG (50 µg/kg body weight) significantly inhibited the growth of FaDu xenografts in athymic nude mice. In immunohistochemical analysis, the xenografts from AGG-treated mice displayed a decrease in PCNA expression and an increase in caspase-3 activation as compared to the controls. In conclusion, we established a connection among ROS, ATM and p73 in AGG-induced apoptosis, which might be useful in enhancing the therapeutic targeting of p53 deficient oral squamous cell carcinoma.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/uso terapêutico
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Carcinoma de Células Escamosas/tratamento farmacológico
Dano ao DNA/efeitos dos fármacos
Neoplasias Bucais/tratamento farmacológico
Lectinas de Plantas/uso terapêutico
Proteína Tumoral p73/metabolismo
[Mh] Termos MeSH secundário: Abrus/química
Animais
Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Camundongos
Camundongos Nus
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Modelos Moleculares
Boca/efeitos dos fármacos
Boca/metabolismo
Boca/patologia
Neoplasias Bucais/metabolismo
Neoplasias Bucais/patologia
Lectinas de Plantas/química
Lectinas de Plantas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Plant Lectins); 0 (Reactive Oxygen Species); 0 (Tumor Protein p73); 0 (abrus agglutinin); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22679


  3 / 93 MEDLINE  
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[PMID]:28288940
[Au] Autor:Jeong YH; Park JS; Kim DH; Kang JL; Kim HS
[Ad] Endereço:Department of Molecular Medicine, Tissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 158-710, South Korea.
[Ti] Título:Anti-inflammatory mechanism of lonchocarpine in LPS- or poly(I:C)-induced neuroinflammation.
[So] Source:Pharmacol Res;119:431-442, 2017 May.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuroinflammation plays an important role in the progression of various neurodegenerative diseases. In this study, we investigated the anti-inflammatory effects of lonchocarpine, a natural compound isolated from Abrus precatorius, under in vitro and in vivo neuroinflammatory conditions induced by challenge with lipopolysaccharide (LPS)- or polyinosinic-polycytidylic acid (poly(I:C)). Lonchocarpine suppressed the expression of iNOS and proinflammatory cytokines in LPS or poly(I:C)-stimulated BV2 microglial cells. These anti-inflammatory effects were verified in brains of mice with systemic inflammation induced by administration of LPS or poly(I:C). Lonchocarpine reduced the number of Iba-1-positive activated microglia, and suppressed the mRNA expression of various proinflammatory markers in the cortex of LPS- or poly(I:C)-injected mice. Molecular mechanistic experiments showed that lonchocarpine inhibited NF-κB activity by reducing the phosphorylation and degradation of IκBα in LPS- or poly(I:C)-stimulated BV2 cells. Analysis of further upstream signaling pathways in LPS-stimulated microglia showed that lonchocarpine inhibited the phosphorylation of IκB kinase and TGFß-activated kinase 1 (TAK1). Moreover, lonchocarpine suppressed the interaction of myeloid differentiation factor 88 (MyD88) and intereleukin-1 receptor-associated kinase 4 (IRAK4). These data suggest that toll-like receptor 4 downstream signals such as MyD88/IRAK4-TAK1-NF-κB are at least partly involved in the anti-inflammatory mechanism of lonchocarpine in LPS-stimulated microglia. Its strong anti-inflammatory effects may make lonchocarpine an effective preventative drug for neuroinflammatory disorders that are associated with systemic inflammation.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Benzopiranos/farmacologia
Chalconas/farmacologia
Inflamação/tratamento farmacológico
Lipopolissacarídeos/imunologia
Microglia/efeitos dos fármacos
Poli I-C/imunologia
[Mh] Termos MeSH secundário: Abrus/química
Animais
Anti-Inflamatórios/química
Anti-Inflamatórios/isolamento & purificação
Benzopiranos/química
Benzopiranos/isolamento & purificação
Linhagem Celular
Chalconas/química
Chalconas/isolamento & purificação
Inflamação/imunologia
Interleucina-10/imunologia
Interleucina-6/imunologia
Camundongos
Microglia/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Benzopyrans); 0 (Chalcones); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Tumor Necrosis Factor-alpha); 0 (lonchocarpine); 130068-27-8 (Interleukin-10); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE


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[PMID]:28288935
[Au] Autor:Sant B; Rao PV; Nagar DP; Pant SC; Bhasker AS
[Ad] Endereço:Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Jhansi Road, Gwalior 474002, India.
[Ti] Título:Evaluation of abrin induced nephrotoxicity by using novel renal injury markers.
[So] Source:Toxicon;131:20-28, 2017 Jun 01.
[Is] ISSN:1879-3150
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abrin is a potent plant toxin analogous to ricin that is derived from the seeds of Abrus precatorius plant. It belongs to the family of type II ribosome-inactivating proteins and causes cell death by irreversibly inactivating ribosomes through site-specific depurination. In this study we examined the in vivo nephrotoxicity potential of abrin toxin in terms of oxidative stress, inflammation, histopathological changes and biomarkers of kidney injury. Animals were exposed to 0.5 and 1.0 LD50 dose of abrin by intraperitoneal route and observed for 1, 3, and 7 day post-toxin exposure. Depletion of reduced glutathione and increased lipid peroxidation levels were observed in abrin treated mice. In addition, abrin also induced inflammation in the kidneys as observed through expression of MMP-9 and MMP-9/NGAL complex in abrin treated groups by using zymography method. Nephrotoxicity was also evaluated by western blot analysis of kidney injury biomarkers including Clusterin, Cystatin C and NGAL, and their results indicate severity of kidney injury in abrin treated groups. Kidney histology confirmed inflammatory changes due to abrin. The data generated in the present study clearly prove the nephrotoxicity potential of abrin.
[Mh] Termos MeSH primário: Abrina/toxicidade
Biomarcadores/sangue
Nefropatias/patologia
Rim/efeitos dos fármacos
[Mh] Termos MeSH secundário: Abrus/química
Animais
Glutationa/sangue
Inflamação/induzido quimicamente
Inflamação/patologia
Rim/patologia
Nefropatias/induzido quimicamente
Peroxidação de Lipídeos/efeitos dos fármacos
Lipocalina-2/genética
Lipocalina-2/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Estresse Oxidativo/efeitos dos fármacos
Sementes/química
Toxinas Biológicas/toxicidade
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Lipocalin-2); 0 (Toxins, Biological); 0 (Tumor Necrosis Factor-alpha); 126469-30-5 (Lcn2 protein, mouse); 1393-62-0 (Abrin); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE


  5 / 93 MEDLINE  
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[PMID]:28189973
[Au] Autor:Jang HM; Kang GD; Van Le TK; Lim SM; Jang DS; Kim DH
[Ad] Endereço:Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea; Department of Pharmacy, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
[Ti] Título:4-Methoxylonchocarpin attenuates inflammation by inhibiting lipopolysaccharide binding to Toll-like receptor of macrophages and M1 macrophage polarization.
[So] Source:Int Immunopharmacol;45:90-97, 2017 Apr.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The roots of Abrus precatorius (AP, Fabaceae) have traditionally been used in Vietnam and China for the treatment of inflammatory diseases such as stomatitis, asthma, bronchitis, and hepatitis. Therefore, in this study, we isolated 4-methoxylonchocarpin (ML), an anti-inflammatory compound present in AP, and studied its anti-inflammatory effects in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. In lipopolysaccharide (LPS)-stimulated macrophages, ML was found to inhibit nuclear factor (NF)-κB activation and tumor necrosis factor (TNF) and interleukin (IL)-6 expression by inhibiting LPS binding to Toll-like receptor 4 (TLR4) in vitro. Oral administration of ML in mice with TNBS-induced colitis suppressed colon shortening and colonic myeloperoxidase activity. ML treatment significantly inhibited the activation of nuclear factor (NF)-κB and phosphorylation of transforming growth factor ß-activated kinase 1 in the colon. Treatment with ML also inhibited TNBS-induced expression of IL-1ß, IL-17A, and TNF. While ML reduced the TNBS-induced expression of M1 macrophage markers such as arginase-2 and TNF, it was found to increase the expression of M2 macrophage markers such as arginase-1 and IL-10. In conclusion, oral administration of ML attenuated colitis in mice by inhibiting the binding of LPS to TLR4 on immune cells and increasing the polarization of M1 macrophages to M2 macrophages.
[Mh] Termos MeSH primário: Abrus/imunologia
Anti-Inflamatórios/uso terapêutico
Colite/tratamento farmacológico
Colo/efeitos dos fármacos
Flavonas/uso terapêutico
Inflamação/tratamento farmacológico
Macrófagos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Diferenciação Celular
Células Cultivadas
Colite/induzido quimicamente
Colo/imunologia
Flavonas/química
Inflamação/induzido quimicamente
Interleucina-6
Lipopolissacarídeos/imunologia
Macrófagos/imunologia
Masculino
Camundongos
Camundongos Endogâmicos ICR
NF-kappa B/metabolismo
Receptor 4 Toll-Like/metabolismo
Ácido Trinitrobenzenossulfônico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-hydroxylonchocarpin); 0 (Anti-Inflammatory Agents); 0 (Flavones); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
[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


  6 / 93 MEDLINE  
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[PMID]:28088476
[Au] Autor:Tiwari V; Bagaria S; Karande AA
[Ad] Endereço:Department of Biochemistry, Indian Institute of Science, Bangalore, Karnataka, 560012, India.
[Ti] Título:A chimeric protein of abrin and Abrus precatorius agglutinin that neutralizes abrin mediated lethality in mice.
[So] Source:Toxicon;127:122-129, 2017 Mar 01.
[Is] ISSN:1879-3150
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abrin, a type II ribosome inactivating protein from the Abrus precatorius plant, is extremely toxic. It has been shown to be 75 times more potent than its infamous sister toxin, ricin and their potential use in bio-warfare is a cause of major concern. Although several vaccine candidates are under clinical trials for ricin, none are available against abrin. The present study proposes a chimeric protein, comprising of 1-123 amino acids taken from the A chain of abrin and 124-175 amino acids from Abrus precatorius agglutinin A chain, as a vaccine candidate against abrin intoxication. The design was based on the inclusion of the immunogenic region of the full length protein and the minimal essential folding domains required for inducing neutralizing antibody response. The chimera also contains the epitope for the only two neutralizing antibodies; D6F10 and A7C4, reported against abrin till now. Active immunization with the chimera protected all the mice challenged with 45 X LD of abrin. Also, passive transfer of antibodies raised against the chimera rescued all mice challenged with 50 X LD of toxin. Hence the chimeric protein appears to be a promising vaccine candidate against abrin induced lethality.
[Mh] Termos MeSH primário: Abrina/toxicidade
Abrus/química
Aglutininas/imunologia
Lectinas de Plantas/imunologia
Intoxicação por Plantas/prevenção & controle
Proteínas Recombinantes de Fusão/imunologia
[Mh] Termos MeSH secundário: Abrina/genética
Abrus/imunologia
Abrus/envenenamento
Animais
Anticorpos Neutralizantes/genética
Anticorpos Neutralizantes/imunologia
Epitopos
Feminino
Seres Humanos
Células Jurkat
Camundongos Endogâmicos BALB C
Lectinas de Plantas/genética
Intoxicação por Plantas/imunologia
Conformação Proteica
Coelhos
Proteínas Recombinantes de Fusão/genética
Vacinas Sintéticas/genética
Vacinas Sintéticas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agglutinins); 0 (Antibodies, Neutralizing); 0 (Epitopes); 0 (Plant Lectins); 0 (Recombinant Fusion Proteins); 0 (Vaccines, Synthetic); 0 (abrus agglutinin); 1393-62-0 (Abrin)
[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:170116
[St] Status:MEDLINE


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[PMID]:27182794
[Au] Autor:Panda PK; Behera B; Meher BR; Das DN; Mukhopadhyay S; Sinha N; Naik PP; Roy B; Das J; Paul S; Maiti TK; Agarwal R; Bhutia SK
[Ad] Endereço:Department of Life Science, National Institute of Technology, Rourkela, Odisha, India.
[Ti] Título:Abrus Agglutinin, a type II ribosome inactivating protein inhibits Akt/PH domain to induce endoplasmic reticulum stress mediated autophagy-dependent cell death.
[So] Source:Mol Carcinog;56(2):389-401, 2017 Feb.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abrus agglutinin (AGG), a type II ribosome-inactivating protein has been found to induce mitochondrial apoptosis. In the present study, we documented that AGG-mediated Akt dephosphorylation led to ER stress resulting the induction of autophagy-dependent cell death through the canonical pathway in cervical cancer cells. Inhibition of autophagic death with 3-methyladenine (3-MA) and siRNA of Beclin-1 and ATG5 increased AGG-induced apoptosis. Further, inhibiting apoptosis by Z-DEVD-FMK and N-acetyl cysteine (NAC) increased autophagic cell death after AGG treatment, suggesting that AGG simultaneously induced autophagic and apoptotic death in HeLa cells. Additionally, it observed that AGG-induced autophagic cell death in Bax knock down (Bax-KD) and 5-FU resistant HeLa cells, confirming as an alternate cell killing pathway to apoptosis. At the molecular level, AGG-induced ER stress in PERK dependent pathway and inhibition of ER stress by salubrinal, eIF2α phosphatase inhibitor as well as siPERK reduced autophagic death in the presence of AGG. Further, our in silico and colocalization study showed that AGG interacted with pleckstrin homology (PH) domain of Akt to suppress its phosphorylation and consequent downstream mTOR dephosphorylation in HeLa cells. We showed that Akt overexpression could not augment GRP78 expression and reduced autophagic cell death by AGG as compared to pcDNA control, indicating Akt modulation was the upstream signal during AGG's ER stress mediated autophagic cell death. In conclusion, we established that AGG stimulated cell death by autophagy might be used as an alternative tumor suppressor mechanism in human cervical cancer. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Lectinas de Plantas/farmacologia
Domínios de Homologia à Plecstrina/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Inativadoras de Ribossomos Tipo 2/farmacologia
[Mh] Termos MeSH secundário: Abrus/química
Antineoplásicos/isolamento & purificação
Feminino
Células HeLa
Seres Humanos
Modelos Moleculares
Lectinas de Plantas/isolamento & purificação
Proteínas Proto-Oncogênicas c-akt/química
Proteínas Inativadoras de Ribossomos Tipo 2/isolamento & purificação
Neoplasias do Colo do Útero/tratamento farmacológico
Neoplasias do Colo do Útero/metabolismo
Neoplasias do Colo do Útero/patologia
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Plant Lectins); 0 (Ribosome Inactivating Proteins, Type 2); 0 (abrus agglutinin); EC 2.7.11.1 (EIF2AK3 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160517
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22502


  8 / 93 MEDLINE  
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[PMID]:27298272
[Au] Autor:Falach R; Sapoznikov A; Gal Y; Israeli O; Leitner M; Seliger N; Ehrlich S; Kronman C; Sabo T
[Ad] Endereço:Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research, Ness-Ziona, Israel.
[Ti] Título:Quantitative profiling of the in vivo enzymatic activity of ricin reveals disparate depurination of different pulmonary cell types.
[So] Source:Toxicol Lett;258:11-19, 2016 Sep 06.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The plant-derived toxins ricin and abrin, operate by site-specific depurination of ribosomes, which in turn leads to protein synthesis arrest. The clinical manifestation following pulmonary exposure to these toxins is that of a severe lung inflammation and respiratory insufficiency. Deciphering the pathways mediating between the catalytic activity and the developing lung inflammation, requires a quantitative appreciation of the catalytic activity of the toxins, in-vivo. In the present study, we monitored truncated cDNA molecules which are formed by reverse transcription when a depurinated 28S rRNA serves as template. We found that maximal depurination after intranasal exposure of mice to 2LD50 ricin was reached 48h, where nearly 40% of the ribosomes have been depurinated and that depurination can be halted by post-exposure administration of anti-ricin antibodies. We next demonstrated that the effect of ricin intoxication on different cell types populating the lungs differs greatly, and that outstandingly high levels of damage (80% depurination), were observed in particular for pulmonary epithelial cells. Finally, we found that the magnitude of depurination induced by the related plant-derived toxin abrin, was significantly lower in comparison to ricin, and can be attributed mostly to reduced depurination of pulmonary epithelial cells by abrin. This study provides for the first time vital information regarding the scope and timing of the catalytic performance of ricin and abrin in the lungs of intact animals.
[Mh] Termos MeSH primário: Citotoxinas/toxicidade
Pulmão/efeitos dos fármacos
Envenenamento/metabolismo
Inibidores da Síntese de Proteínas/toxicidade
Mucosa Respiratória/efeitos dos fármacos
Ribossomos/efeitos dos fármacos
Ricina/toxicidade
[Mh] Termos MeSH secundário: Abrina/administração & dosagem
Abrina/isolamento & purificação
Abrina/metabolismo
Abrina/toxicidade
Abrus/enzimologia
Administração Intranasal
Animais
Antitoxinas/uso terapêutico
Citotoxinas/administração & dosagem
Citotoxinas/antagonistas & inibidores
Citotoxinas/metabolismo
DNA Complementar/metabolismo
Feminino
Citometria de Fluxo
Dose Letal Mediana
Pulmão/metabolismo
Pulmão/patologia
Camundongos
Pneumonia/etiologia
Pneumonia/prevenção & controle
Envenenamento/tratamento farmacológico
Envenenamento/patologia
Envenenamento/fisiopatologia
Inibidores da Síntese de Proteínas/administração & dosagem
Inibidores da Síntese de Proteínas/química
Inibidores da Síntese de Proteínas/metabolismo
Purinas/metabolismo
RNA Ribossômico 28S/metabolismo
Insuficiência Respiratória/etiologia
Insuficiência Respiratória/prevenção & controle
Mucosa Respiratória/metabolismo
Mucosa Respiratória/patologia
Ribossomos/enzimologia
Ribossomos/metabolismo
Ricina/administração & dosagem
Ricina/antagonistas & inibidores
Ricina/metabolismo
Ricinus/enzimologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antitoxins); 0 (Cytotoxins); 0 (DNA, Complementary); 0 (Protein Synthesis Inhibitors); 0 (Purines); 0 (RNA, Ribosomal, 28S); 1393-62-0 (Abrin); 9009-86-3 (Ricin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE


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[PMID]:27058538
[Au] Autor:Wu S; Fu X; Brennan MA; Brennan CS; Chun C
[Ad] Endereço:College of Light Industry and Food Sciences, South China University of Technology, Guangzhou 510640, China. zemilym87@yahoo.com.
[Ti] Título:The Effects of Different Purifying Methods on the Chemical Properties, in Vitro Anti-Tumor and Immunomodulatory Activities of Abrus cantoniensis Polysaccharide Fractions.
[So] Source:Int J Mol Sci;17(4):511, 2016 Apr 06.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Abrus cantoniensis (Hance) is a popular Chinese vegetable consumed as a beverage, soup or folk medicine. To fully exploit the potential of the polysaccharide in Abrus cantoniensis, nine polysaccharide fractions of Abrus cantoniensis were isolated and purified (AP-AOH30-1, AP-AOH30-2, AP-AOH80-1, AP-AOH80-2, AP-ACl-1, AP-ACl-2, AP-ACl-3, AP-H and AP-L). Fourier-transform infrared spectroscopy (FT-IR) and gas chromatography (GC) were used to characterize these Abrus polysaccharides fractions (APF). In vitro anti-tumor and immunomodulatory activities were also investigated and compared using the rank-sum ratio (RSR) method. Results demonstrated significant differences in the structure and bioactivities among APF, which were associated to the process used for their purification. Among the APF, AP-ACl-3 yield was 613.5 mg/kg of product and consisted of rhamnose (9.8%), arabinose (8.9%), fructose (3.0%), galactose (9.9%), glucose (4.3%), galacturonic acid (3.0%) and glucuronic acid (61.1%) with a molecular weight of 4.4 × 104 Da. Furthermore, AP-ACl-3 exhibited considerable bioactivities significantly preventing the migration of MCF-7 cells and stimulating lymphocyte proliferation along with nitric oxide (NO) production of peritoneal macrophages. AP-ACl-3 could be explored as a novel potential anti-tumor and immunomodulatory agent.
[Mh] Termos MeSH primário: Abrus/química
Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/farmacologia
Fatores Imunológicos/química
Fatores Imunológicos/farmacologia
Polissacarídeos/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Fitogênicos/isolamento & purificação
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Fatores Imunológicos/isolamento & purificação
Linfócitos/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Masculino
Camundongos Endogâmicos BALB C
Neoplasias/tratamento farmacológico
Polissacarídeos/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Immunologic Factors); 0 (Polysaccharides)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160409
[St] Status:MEDLINE


  10 / 93 MEDLINE  
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Texto completo
[PMID]:27057623
[Au] Autor:Wu S; Fu X; You L; Abbasi AM; Meng H; Liu D; Aadil RM
[Ad] Endereço:School of Food Science and Engineering, South China University of Technology, Guangzhou 510640, China.
[Ti] Título:Antioxidant, antitumor and immunomodulatory activities of water-soluble polysaccharides in Abrus cantoniensis.
[So] Source:Int J Biol Macromol;89:707-16, 2016 Aug.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Abrus cantoniensis is a vegetative food in tropical areas of Asia and claimed as folk beverages and soups consumed for cleansing liver toxicants and preventing liver diseases. Polysaccharides (ACP-І and ACP-II) were extracted with hot water from A. cantoniensis, and isolated by DEAE cellulose chromatography. The chemical properties as well as antioxidant, antitumor and immunomodulatory activities of ACP-I and ACP-II were investigated. The results showed that the ACP-I (9.09kDa) contained only glucose and ACP-II (38.45kDa) consisted of rhamnose, arabinose, galactose and glucose. ACP-II exhibited higher oxygen radical absorbance capacity (ORAC) and hydroxyl radical prevention capacity (HRPC) than ACP-I with ORAC values and HRPC values of 53.42±3.32µmol Trolox equiv./g DW and 34.84±5.07µmol Trolox equiv./g DW. Besides, in the wound healing assay, ACP-II exhibited potent migration inhibitory effects on MCF-7 cells. ACP-II could also significantly stimulate the proliferation of splenocytes and thymocytes, and enhanced NO production of peritoneal macrophages. These findings suggest that the polysaccharide ACP-II in A. cantoniensis could be served as a novel potential functional food.
[Mh] Termos MeSH primário: Abrus/química
Antineoplásicos/administração & dosagem
Antioxidantes/administração & dosagem
Extratos Vegetais/administração & dosagem
[Mh] Termos MeSH secundário: Antineoplásicos/química
Antioxidantes/química
Neoplasias da Mama/tratamento farmacológico
Feminino
Seres Humanos
Fatores Imunológicos/administração & dosagem
Fatores Imunológicos/química
Células MCF-7
Extratos Vegetais/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Antioxidants); 0 (Immunologic Factors); 0 (Plant Extracts)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170302
[Lr] Data última revisão:
170302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160409
[St] Status:MEDLINE



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