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[PMID]:29329002
[Au] Autor:Durdagi S; Aksoydan B; Erol I; Kantarcioglu I; Ergun Y; Bulut G; Acar M; Avsar T; Liapakis G; Karageorgos V; Salmas RE; Sergi B; Alkhatib S; Turan G; Yigit BN; Cantasir K; Kurt B; Kilic T
[Ad] Endereço:Computational Biology and Molecular Simulations Laboratory, Department of Biophysics, School of Medicine, Bahcesehir University (BAU), Istanbul, Turkey; Neuroscience Program, Graduate School of Health Sciences, Bahcesehir University, Istanbul, Turkey. Electronic address: serdar.durdagi@med.bau.edu.t
[Ti] Título:Integration of multi-scale molecular modeling approaches with experiments for the in silico guided design and discovery of novel hERG-Neutral antihypertensive oxazalone and imidazolone derivatives and analysis of their potential restrictive effects on cell proliferation.
[So] Source:Eur J Med Chem;145:273-290, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:AT1 antagonists is the most recent drug class of molecules against hypertension and they mediate their actions through blocking detrimental effects of angiotensin II (A-II) when acts on type I (AT1) A-II receptor. The effects of AT1 antagonists are not limited to cardiovascular diseases. AT1 receptor blockers may be used as potential anti-cancer agents - due to the inhibition of cell proliferation stimulated by A-II. Therefore, AT1 receptors and the A-II biosynthesis mechanisms are targets for the development of new synthetic drugs and therapeutic treatment of various cardiovascular and other diseases. In this work, multi-scale molecular modeling approaches were performed and it is found that oxazolone and imidazolone derivatives reveal similar/better interaction energy profiles compared to the FDA approved sartan molecules at the binding site of the AT1 receptor. In silico-guided designed hit molecules were then synthesized and tested for their binding affinities to human AT1 receptor in radioligand binding studies, using [ I-Sar -Ile ] AngII. Among the compounds tested, 19d and 9j molecules bound to receptor in a dose response manner and with relatively high affinities. Next, cytotoxicity and wound healing assays were performed for these hit molecules. Since hit molecule 19d led to deceleration of cell motility in all three cell lines (NIH3T3, A549, and H358) tested in this study, this molecule is investigated in further tests. In two cell lines (HUVEC and MCF-7) tested, 19d induced G2/M cell cycle arrest in a concentration dependent manner. Adherent cells detached from the plates and underwent cell death possibly due to apoptosis at 19d concentrations that induced cell cycle arrest.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Antineoplásicos/farmacologia
Descoberta de Drogas
Canais de Potássio Éter-A-Go-Go/antagonistas & inibidores
Imidazóis/farmacologia
Oxazolona/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/síntese química
Anti-Hipertensivos/química
Antineoplásicos/síntese química
Antineoplásicos/química
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Morte Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Canais de Potássio Éter-A-Go-Go/metabolismo
Seres Humanos
Imidazóis/síntese química
Imidazóis/química
Camundongos
Modelos Moleculares
Estrutura Molecular
Células NIH 3T3
Oxazolona/síntese química
Oxazolona/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Antineoplastic Agents); 0 (Ether-A-Go-Go Potassium Channels); 0 (Imidazoles); 0 (KCNH1 protein, human); 0 (imidazolone); 15646-46-5 (Oxazolone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  2 / 1001 MEDLINE  
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[PMID]:29330048
[Au] Autor:Watabe T; Nagaishi T; Tsugawa N; Kojima Y; Jose N; Hosoya A; Onizawa M; Nemoto Y; Oshima S; Nakamura T; Karasuyama H; Adachi T; Watanabe M
[Ad] Endereço:Department of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
[Ti] Título:B cell activation in the cecal patches during the development of an experimental colitis model.
[So] Source:Biochem Biophys Res Commun;496(2):367-373, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although previous studies have suggested that appendix seems to be involved in the colitis, the role of this in the pathogenesis remains unclear. In this study, we assessed the importance of appendiceal lymphoid follicles, specifically the cecal patches (CP) in mice, using an experimental colitis model. Treatment with oxazolone resulted in ulcerations particularly at CP with follicular expansion as well as colitis. The colitis was attenuated by either appendectomy or the absence of mature B cells. We therefore established an intravital imaging system accompanied by the fluorescence resonance energy transfer technology to analyze the dynamic immune response of CP B cells. Our observation revealed frequent Ca signaling in CP B cells during the early phase of colitis development. These findings suggested that the CP B cells may be involved in the pathogenesis of colitis including inflammatory bowel diseases in humans.
[Mh] Termos MeSH primário: Apêndice/imunologia
Ceco/imunologia
Colite/imunologia
Colo/imunologia
Estruturas Linfoides Terciárias/imunologia
[Mh] Termos MeSH secundário: Animais
Apêndice/diagnóstico por imagem
Apêndice/patologia
Linfócitos B/imunologia
Linfócitos B/patologia
Sinalização do Cálcio
Ceco/diagnóstico por imagem
Ceco/patologia
Colite/induzido quimicamente
Colite/diagnóstico por imagem
Colite/patologia
Colo/diagnóstico por imagem
Colo/patologia
Modelos Animais de Doenças
Seres Humanos
Microscopia Intravital
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Oxazolona
Estruturas Linfoides Terciárias/diagnóstico por imagem
Estruturas Linfoides Terciárias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
15646-46-5 (Oxazolone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE


  3 / 1001 MEDLINE  
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[PMID]:29353040
[Au] Autor:Jung Y; Kim JC; Park NJ; Bong SK; Lee S; Jegal H; Jin LT; Kim SM; Kim YK; Kim SN
[Ad] Endereço:Natural Products Research Institute, Korea Institute of Science and Technology, Gangneung, Gangwon-do 25451, Republic of Korea.
[Ti] Título:Eupatilin, an activator of PPARα, inhibits the development of oxazolone-induced atopic dermatitis symptoms in Balb/c mice.
[So] Source:Biochem Biophys Res Commun;496(2):508-514, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone) is the main lipophilic flavonoid obtained from the Artemisia species. Eupatilin has been reported to have anti-apoptotic, anti-oxidative and anti-inflammatory activities. Previously, we found that eupatilin increases transcriptional activity and expression of peroxisome proliferator-activated receptor α (PPARα) in a keratinocyte cell line and acts as an agonist of PPARα. PPARα agonists ameliorate atopic dermatitis (AD) and restore the skin barrier function. In this study, we confirmed that the effects of eupatilin improved AD-like symptoms in an oxazolone-induced AD-like mouse model. Furthermore, we found that eupatilin suppressed the levels of serum immunoglobulin E (IgE), interleukin-4 (IL-4), and AD involved cytokines, such as tumor necrosis factor α (TNFα), interferon-γ (IFN-γ), IL-1ß, and thymic stromal lymphopoietin (TSLP), IL-33, IL-25 and increased the levels of filaggrin and loricrin in the oxazolone-induced AD-like mouse model. Taken together, our data suggest that eupatilin is a potential candidate for the treatment of AD.
[Mh] Termos MeSH primário: Dermatite Atópica/tratamento farmacológico
Fármacos Dermatológicos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Flavonoides/farmacologia
PPAR alfa/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Citocinas/genética
Citocinas/imunologia
Dermatite Atópica/induzido quimicamente
Dermatite Atópica/imunologia
Dermatite Atópica/patologia
Relação Dose-Resposta a Droga
Feminino
Regulação da Expressão Gênica
Imunoglobulina E/sangue
Imunoglobulina E/genética
Interferon gama/genética
Interferon gama/imunologia
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-33/genética
Interleucina-33/imunologia
Interleucina-4/genética
Interleucina-4/imunologia
Interleucinas/genética
Interleucinas/imunologia
Proteínas de Filamentos Intermediários/genética
Proteínas de Filamentos Intermediários/imunologia
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Oxazolona
PPAR alfa/imunologia
Ratos
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (D17Wsu104e protein, mouse); 0 (Dermatologic Agents); 0 (Drugs, Chinese Herbal); 0 (Flavonoids); 0 (IL1B protein, mouse); 0 (Il33 protein, mouse); 0 (Interleukin-1beta); 0 (Interleukin-33); 0 (Interleukins); 0 (Intermediate Filament Proteins); 0 (Membrane Proteins); 0 (PPAR alpha); 0 (Tumor Necrosis Factor-alpha); 0 (filaggrin); 0 (loricrin); 0 (thymic stromal lymphopoietin); 15646-46-5 (Oxazolone); 207137-56-2 (Interleukin-4); 37341-29-0 (Immunoglobulin E); 4D58O05490 (eupatilin); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


  4 / 1001 MEDLINE  
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[PMID]:27776738
[Au] Autor:Cheng Z; Peng HL; Zhang R; Fu XM; Zhang GS
[Ad] Endereço:Department of Hematology, Institute of Molecular Hematology, The Second Xiang-ya Hospital, Central South University, Changsha, Hunan, PR China.
[Ti] Título:Bone marrow-derived innate macrophages attenuate oxazolone-induced colitis.
[So] Source:Cell Immunol;311:46-53, 2017 Jan.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that a subpopulation of granulocyte macrophage colony-stimulating factor (GM-CSF)-dependent F4/80 CD11b innate macrophages could be derived from bone marrow cells by continuous in vitro culturing. These cells could be induced to differentiate into M1 or M2 macrophages in vitro. In the current study, we sought to determine whether bone marrow cell-derived innate macrophages (BMIMs) could be used to fulfill an anti-inflammatory purpose by intravenous transplantation in vivo after being stimulated to differentiate into M2 macrophages. Because Th2 cytokines, such as interleukin IL-4 and IL-13, can induce macrophage polarization into M2 macrophages, we treated the BMIMs with IL-4 and IL-13 in vitro. Next, the M2 macrophages were intravenously transplanted into a typical Th2-mediated inflammatory disease model, oxazolone (OXZ)-induced colitis, to assess the anti-inflammatory activity of BMIM-derived M2 macrophages (BMIM-M2Ms) in vivo. After transplantation, the severity of intestinal inflammation was attenuated. In addition, colon lengths and mouse body weights were noticeably improved. F4/80 CD206 double-positive cells (displaying the markers of M2 macrophages) had accumulated in the colon tissue of BMIM-M2M-transplanted mice. This evidence demonstrated that bone marrow-derived BMIM-M2Ms could be used to alleviate OXZ-induced Th2-mediated inflammation in a mouse model in vivo.
[Mh] Termos MeSH primário: Colite/imunologia
Colite/terapia
Macrófagos/transplante
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/metabolismo
Antígeno CD11b/metabolismo
Células Cultivadas
Colite/induzido quimicamente
Citocinas/metabolismo
Modelos Animais de Doenças
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Seres Humanos
Imunidade Inata
Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Oxazolona
Fenótipo
Receptores de Superfície Celular/metabolismo
Células Th2/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CD11b Antigen); 0 (Cytokines); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (mannose receptor); 0 (monocyte-macrophage differentiation antigen); 15646-46-5 (Oxazolone); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171217
[Lr] Data última revisão:
171217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  5 / 1001 MEDLINE  
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[PMID]:28935759
[Au] Autor:Karlsen TV; Reikvam T; Tofteberg A; Nikpey E; Skogstrand T; Wagner M; Tenstad O; Wiig H
[Ad] Endereço:From the Department of Biomedicine, University of Bergen, Norway (T.V.K., T.R., A.T., E.N., T.S., M.W., O.T., H.W.); and Departments of Medicine (E.N.) and Pathology (M.W.), Haukeland University Hospital, Bergen, Norway. tine.karlsen@uib.no helge.wiig@uib.no.
[Ti] Título:Lymphangiogenesis Facilitates Initial Lymph Formation and Enhances the Dendritic Cell Mobilizing Chemokine CCL21 Without Affecting Migration.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2128-2135, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Lymphatic vessels play an important role in body fluid, as well as immune system homeostasis. Although the role of malfunctioning or missing lymphatics has been studied extensively, less is known on the functional consequences of a chronically expanded lymphatic network or lymphangiogenesis. APPROACH AND RESULTS: To this end, we used K14-VEGF-C (keratin-14 vascular endothelial growth factor-C) transgenic mice overexpressing the vascular endothelial growth factor C in skin and investigated the responses to inflammatory and fluid volume challenges. We also recorded interstitial fluid pressure, a major determinant of lymph flow. Transgenic mice had a strongly enhanced lymph vessel area in skin. Acute inflammation induced by lipopolysaccharide and chronic inflammation by delayed-type hypersensitivity both resulted in increased interstitial fluid pressure and reduced lymph flow, both to the same extent in wild-type and transgenic mice. Hyperplastic lymphatic vessels, however, demonstrated enhanced transport capacity after local fluid overload not induced by inflammation. In this situation, interstitial fluid pressure was increased to a similar extent in the 2 strains, thus, suggesting that the enhanced lymph vessel area facilitated initial lymph formation. The increased lymph vessel area resulted in an enhanced production of the chemoattractant CCL21 that, however, did not result in augmented dendritic cell migration after induction of local skin inflammation by fluorescein isothiocyanate. CONCLUSIONS: An expanded lymphatic network is capable of enhanced chemoattractant production, and lymphangiogenesis will facilitate initial lymph formation favoring increased clearance of fluid in situations of augmented fluid filtration.
[Mh] Termos MeSH primário: Quimiocina CCL21/metabolismo
Quimiotaxia
Células Dendríticas/metabolismo
Dermatite Alérgica de Contato/metabolismo
Linfa/metabolismo
Linfangiogênese
Vasos Linfáticos/metabolismo
Linfedema/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite Alérgica de Contato/genética
Dermatite Alérgica de Contato/patologia
Dermatite Alérgica de Contato/fisiopatologia
Modelos Animais de Doenças
Líquido Extracelular/metabolismo
Feminino
Deslocamentos de Líquidos Corporais
Fluoresceína-5-Isotiocianato
Genótipo
Queratina-14/genética
Lipopolissacarídeos
Vasos Linfáticos/patologia
Vasos Linfáticos/fisiopatologia
Linfedema/genética
Linfedema/patologia
Linfedema/fisiopatologia
Masculino
Camundongos Endogâmicos C3H
Camundongos Transgênicos
Oxazolona
Fenótipo
Pressão
Regiões Promotoras Genéticas
Transdução de Sinais
Fatores de Tempo
Regulação para Cima
Fator C de Crescimento do Endotélio Vascular/genética
Fator C de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21); 0 (Keratin-14); 0 (Lipopolysaccharides); 0 (Vascular Endothelial Growth Factor C); 15646-46-5 (Oxazolone); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309883


  6 / 1001 MEDLINE  
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[PMID]:28912045
[Au] Autor:Figliuolo VR; Dos Santos LM; Abalo A; Nanini H; Santos A; Brittes NM; Bernardazzi C; de Souza HSP; Vieira LQ; Coutinho-Silva R; Coutinho CMLM
[Ad] Endereço:Instituto de Biofísica Carlos Chagas Filho - IBCCF, Universidade Federal do Rio de Janeiro, RJ, Brazil; Laboratório de Inovações em Terapias, Ensino e Bioprodutos - LITEB, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, RJ, Brazil.
[Ti] Título:Sulfate-reducing bacteria stimulate gut immune responses and contribute to inflammation in experimental colitis.
[So] Source:Life Sci;189:29-38, 2017 Nov 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The intestinal microbiota is critical for mammalian immune system development and homeostasis. Sulfate-reducing bacteria (SRB) are part of the normal gut microbiota, but their increased levels may contribute to colitis development, likely in association with hydrogen sulfide (H S) production. Here, we investigated the effects of SRB in the gut immune response in germ-free mice, and in experimental colitis. After 7days of colonization with Desulfovibrio indonesiensis or with a human SRB consortium (from patients with colitis), germ-free mice exhibited alterations in the colonic architecture, with increased cell infiltration in the lamina propria. SRB colonization upregulated the Th17 and Treg profiles of cytokine production/cell activation, in T cells from mesenteric lymph nodes. These alterations were more pronounced in mice colonized with the human SRB consortium, although D. indonesiensis colonization produced higher levels of H S. Importantly, the colon of C57BL/6 mice with colitis induced by TNBS or oxazolone had increased SRB colonization, and the administration of D. indonesiensis to mice with TNBS-induced colitis clearly exacerbated the alterations in colonic architecture observed in the established disease, and also increased mouse weight loss. We conclude that SRB contribute to immune response activation in the gut and play an important role in colitis development.
[Mh] Termos MeSH primário: Colite/patologia
Desulfovibrio/metabolismo
Inflamação/patologia
Sulfatos/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/imunologia
Modelos Animais de Doenças
Feminino
Seres Humanos
Inflamação/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Oxazolona/toxicidade
Linfócitos T Reguladores/imunologia
Células Th17/imunologia
Ácido Trinitrobenzenossulfônico/toxicidade
Perda de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sulfates); 15646-46-5 (Oxazolone); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


  7 / 1001 MEDLINE  
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[PMID]:28826779
[Au] Autor:Tsuchiyama H; Maeda A; Nakajima M; Kitsukawa M; Takahashi K; Miyoshi T; Mutsuga M; Asaoka Y; Miyamoto Y; Oshida K
[Ad] Endereço:Pharmaceutical Research Laboratories, Toray Industries Inc., 10-1, Tebiro 6-chome, Kamakura, Kanagawa, 248-8555, Japan.
[Ti] Título:Gene expression profiles in auricle skin as a possible additional endpoint for determination of sensitizers: A multi-endpoint evaluation of the local lymph node assay.
[So] Source:Toxicol Lett;280:133-141, 2017 Oct 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The murine local lymph node assay (LLNA) is widely used to test chemicals to induce skin sensitization. Exposure of mouse auricle skin to a sensitizer results in proliferation of local lymph node T cells, which has been measured by in vivo incorporation of H -methyl thymidine or 5-bromo-2'-deoxyuridine (BrdU). The stimulation index (SI), the ratio of the mean proliferation in each treated group to that in the concurrent vehicle control group, is frequently used as a regulatory-authorized endpoint for LLNA. However, some non-sensitizing irritants, such as sodium dodecyl sulfate (SDS) or methyl salicylate (MS), have been reported as false-positives by this endpoint. In search of a potential endpoint to enhance the specificity of existing endpoints, we evaluated 3 contact sensitizers; (hexyl cinnamic aldehyde [HCA], oxazolone [OXA], and 2,4-dinitrochlorobenzene [DNCB]), 1 respiratory sensitizer (toluene 2,4-diisocyanate [TDI]), and 2 non-sensitizing irritants (MS and SDS) by several endpoints in LLNA. Each test substance was applied to both ears of female CBA/Ca mice daily for 3 consecutive days. The ears and auricle lymph node cells were analyzed on day 5 for endpoints including the SI value, lymph node cell count, cytokine release from lymph node cells, and histopathological changes and gene expression profiles in auricle skin. The SI values indicated that all the test substances induced significant proliferation of lymph node cells. The lymph node cell counts showed no significant changes by the non-sensitizers assessed. The inflammatory findings of histopathology were similar among the auricle skins treated by sensitizers and irritants. Gene expression profiles of cytokines IFN-γ, IL-4, and IL-17 in auricle skin were similar to the cytokine release profiles in draining lymph node cells. In addition, the gene expression of the chemokine CXCL1 and/or CXCL2 showed that it has the potential to discriminate sensitizers and non-sensitizing irritants. Our results suggest that multi-endpoint analysis in the LLNA leads to a better determination of the sensitizing potential of test substances. We also show that the gene expression of CXCL1 and/or CXCL2, which is involved in elicitation of contact hypersensitivity (CHS), can be a possible additional endpoint for discrimination of sensitizing compounds in LLNA.
[Mh] Termos MeSH primário: Pavilhão Auricular/metabolismo
Ensaio Local de Linfonodo
Pele/metabolismo
Transcriptoma/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/metabolismo
Dinitroclorobenzeno/toxicidade
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos CBA
Oxazolona/toxicidade
Salicilatos/toxicidade
Dodecilsulfato de Sódio/toxicidade
Tolueno 2,4-Di-Isocianato/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Salicylates); 15646-46-5 (Oxazolone); 17X7AFZ1GH (Toluene 2,4-Diisocyanate); 368GB5141J (Sodium Dodecyl Sulfate); 78243HXH5O (2,6-diisocyanatotoluene); GE3IBT7BMN (Dinitrochlorobenzene); LAV5U5022Y (methyl salicylate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


  8 / 1001 MEDLINE  
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[PMID]:28607110
[Au] Autor:Biagioli M; Carino A; Cipriani S; Francisci D; Marchianò S; Scarpelli P; Sorcini D; Zampella A; Fiorucci S
[Ad] Endereço:Department of Surgical and Biomedical Sciences, University of Perugia, Perugia 06132, Italy.
[Ti] Título:The Bile Acid Receptor GPBAR1 Regulates the M1/M2 Phenotype of Intestinal Macrophages and Activation of GPBAR1 Rescues Mice from Murine Colitis.
[So] Source:J Immunol;199(2):718-733, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GPBAR1 (TGR5 or M-BAR) is a G protein-coupled receptor for secondary bile acids that is highly expressed in monocytes/macrophages. In this study, we aimed to determine the role of GPBAR1 in mediating leukocyte trafficking in chemically induced models of colitis and investigate the therapeutic potential of BAR501, a small molecule agonist for GPBAR1. These studies demonstrated that GPBAR1 gene ablation enhanced the recruitment of classically activated macrophages in the colonic lamina propria and worsened the severity of inflammation. In contrast, GPBAR1 activation by BAR501 reversed intestinal inflammation in the trinitrobenzenesulfonic acid and oxazolone models by reducing the trafficking of Ly6C monocytes from blood to intestinal mucosa. Exposure to BAR501 shifted intestinal macrophages from a classically activated (CD11b , CCR7 , F4/80 ) to an alternatively activated (CD11b , CCR7 , F4/80 ) phenotype, reduced the expression of inflammatory genes (TNF-α, IFN-γ, IL-1ß, IL-6, and CCL2 mRNAs), and attenuated the wasting syndrome and severity of colitis (≈70% reduction in the Colitis Disease Activity Index). The protective effect was lost in Gpbar1 mice. Exposure to BAR501 increased the colonic expression of IL-10 and TGF-ß mRNAs and the percentage of CD4 /Foxp3 cells. The beneficial effects of BAR501 were lost in Il-10 mice. In a macrophage cell line, regulation of IL-10 by BAR501 was GPBAR1 dependent and was mediated by the recruitment of CREB to its responsive element in the IL-10 promoter. In conclusion, GPBAR1 is expressed in circulating monocytes and colonic macrophages, and its activation promotes a IL-10-dependent shift toward an alternatively activated phenotype. The targeting of GPBAR1 may offer therapeutic options in inflammatory bowel diseases.
[Mh] Termos MeSH primário: Colite/imunologia
Regulação da Expressão Gênica/imunologia
Mucosa Intestinal/imunologia
Macrófagos/imunologia
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/genética
Antígenos Ly/imunologia
Linhagem Celular
Movimento Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Colestanóis/administração & dosagem
Colestanóis/farmacologia
Colite/induzido quimicamente
Colite/metabolismo
Inflamação/imunologia
Interleucina-10/deficiência
Interleucina-10/genética
Interleucina-10/imunologia
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-6/genética
Interleucina-6/imunologia
Ativação de Macrófagos
Macrófagos/efeitos dos fármacos
Camundongos
Membrana Mucosa/imunologia
Oxazolona/administração & dosagem
Fenótipo
Regiões Promotoras Genéticas
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/deficiência
Receptores Acoplados a Proteínas-G/genética
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Ácido Trinitrobenzenossulfônico/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-ethyl-3,7-dihydroxycholan-24-ol); 0 (Antigens, Ly); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Cholestanols); 0 (Gpbar1 protein, mouse); 0 (IL10 protein, mouse); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Ly-6C antigen, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Tumor Necrosis Factor-alpha); 0 (interleukin-6, mouse); 130068-27-8 (Interleukin-10); 15646-46-5 (Oxazolone); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700183


  9 / 1001 MEDLINE  
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[PMID]:28569761
[Au] Autor:Wirtz S; Popp V; Kindermann M; Gerlach K; Weigmann B; Fichtner-Feigl S; Neurath MF
[Ad] Endereço:Department of Medicine 1, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany.
[Ti] Título:Chemically induced mouse models of acute and chronic intestinal inflammation.
[So] Source:Nat Protoc;12(7):1295-1309, 2017 Jul.
[Is] ISSN:1750-2799
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammatory bowel diseases (IBDs) result in diarrhea and abdominal pain with further potential complications such as tissue fibrosis and stenosis. Animal models help in understanding the immunopathogenesis of IBDs and in the design of novel therapeutic concepts. Here we present an updated version of a protocol we published in 2007 for key models of acute and chronic forms of colitis induced by 2,4,6-trinitro-benzene sulfonic acid (TNBS), oxazolone and dextran sulfate sodium (DSS). This protocol update describes an adaptation of the existing protocol that modifies the technique. This protocol has been used to generate improved mouse models that better reflect the nature of IBDs in humans. In TNBS and oxazolone colitis models, topical administration of hapten reagents results in T-cell-mediated immunity against haptenized proteins and luminal antigens. By contrast, to generate DSS colitis models, mice orally receive DSS, causing death of epithelial cells, compromising barrier function and causing subsequent inflammation. The analysis of the acute colitis models can be performed within 1-2 weeks, whereas that of the chronic models may take 2-4 months. The strengths of the acute models are that they are based on the analysis of short-lasting barrier alterations, innate immune effects and flares. The advantages of the chronic models are that they may offer better insight into adaptive immunity and complications such as neoplasia and tissue fibrosis. The protocol requires basic skills in laboratory animal research.
[Mh] Termos MeSH primário: Colite/induzido quimicamente
Colite/patologia
Modelos Animais de Doenças
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Sulfato de Dextrana/administração & dosagem
Sulfato de Dextrana/toxicidade
Camundongos
Oxazolona/administração & dosagem
Oxazolona/toxicidade
Ácido Trinitrobenzenossulfônico/administração & dosagem
Ácido Trinitrobenzenossulfônico/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
15646-46-5 (Oxazolone); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1038/nprot.2017.044


  10 / 1001 MEDLINE  
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[PMID]:28500957
[Au] Autor:Mohamed LW; El-Badry OM; El-Ansary AK; Ismael A
[Ad] Endereço:Pharmaceutical Organic Chemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Electronic address: lamiawagdy@hotmail.com.
[Ti] Título:Design & synthesis of novel oxazolone & triazinone derivatives and their biological evaluation as COX-2 inhibitors.
[So] Source:Bioorg Chem;72:308-314, 2017 Jun.
[Is] ISSN:1090-2120
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A new series of oxazolones and triazinones were designed and synthesized and evaluated against both COX-1 and COX-2 enzymes. Full structure elucidation of the new derivatives was performed using microanalyses, IR, 1H NMR, 13C NMR and mass spectra. Most of the derivatives showed good inhibitory activity against COX-2 enzyme specifically compounds IIIc, IIIe, IVd and IVg with IC50 values 0.024, 0.019, 0.011 and 0.014µM compared to celecoxib as reference drug with IC50 value of 0.05µM. Altogether, these results indicate that these derivatives can be effective anti-inflammatory agents.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Ciclo-Oxigenase 2/metabolismo
Desenho de Drogas
Oxazolona/farmacologia
Triazinas/farmacologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/síntese química
Anti-Inflamatórios não Esteroides/química
Ciclo-Oxigenase 1/metabolismo
Inibidores de Ciclo-Oxigenase 2/síntese química
Inibidores de Ciclo-Oxigenase 2/química
Relação Dose-Resposta a Droga
Estrutura Molecular
Oxazolona/química
Relação Estrutura-Atividade
Triazinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase 2 Inhibitors); 0 (Triazines); 15646-46-5 (Oxazolone); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE



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