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[PMID]:29357800
[Au] Autor:Siverio-Mota D; Andujar I; Marrero-Ponce Y; Giner RM; Diaz-Mendoza C; Paba GM; Vicet-Muro L; Cordero-Maldonado ML; de Witte PAM; Crawford AD; Veitia MS; Perez-Jimenez F; Aran VJ
[Ad] Endereço:Laboratory for Molecular Biodiscovery, Department of Pharmaceutical and Pharmacological Sciences, University of Leuven, Herestraat 49, 3000 Leuven, Belgium.
[Ti] Título:Anti-Inflammatory Activity and Cheminformatics Analysis of New Poten t 2-Substituted 1-Methyl-5-Nitroindazolinones.
[So] Source:Curr Top Med Chem;17(30):3236-3248, 2018 Feb 09.
[Is] ISSN:1873-4294
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:After the identification of the anti-inflammatory properties of VA5-13l (2-benzyl-1- methyl-5-nitroindazolinone) in previous investigations, some of its analogous compounds were designed, synthesized and evaluated in two anti-inflammatory methods: LPS-enhanced leukocyte migration assay in zebrafish; and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema. The products evaluated (3, 6, 8, 9 and 10) showed the lower values of relative leukocyte migration at 30 µM (0.14, 0.07, 0.10, 0.13 and 0.07, respectively), while in ear edema and myeloperoxidase activity methods, all the compounds reduced inflammation, only 4 and 16 yielded unsatisfactory results. The relationship linking structure and activity (SAR analysis) was determinate by using SARANEA software. The importance of the 5-Nitro group of the indazole ring for the activity was evident, and showed modest reduction when benzyl (Bn) is changed by alkyl group. A substituted Bn moiety at N2 (R) is the best substituent (5-10); nevertheless, if methylene group of Bn is deleted, the activity is affected. Also, introduction of halogen atoms mainly at positions 3 or 4 of the benzyl moiety (6 and 10) leads in general to strong activities. In fact, compounds 7 and 8 (R = 4-FBn or 4-ClBn, respectively) exhibit satisfactory results in in vivo tests and appear promising. The production of IL-6 at all doses assayed was significantly reduced, except with 16. Nonetheless, the production of TNF-α was significantly inhibited only by this chemical (16) at concentration of 50 µM. On the other hand, compound 2 was the one that mostly inhibited the expression of COX-2 and iNOS. From these results, it can be concluded that the inhibition in the release of cytokines can be one of the mechanisms of action responsible for the anti-inflammatory effect for 2-benzyl derivates while other 2-alkyl derivatives can inhibit production of NO. Therefore, nitroindazolinone chemical prototype could be an interesting structural group with anti-inflammatory purposes in the therapeutic.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Indazóis/farmacologia
Informática
Nitrocompostos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/química
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase 2/química
Relação Dose-Resposta a Droga
Seres Humanos
Indazóis/química
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Estrutura Molecular
Óxido Nítrico/antagonistas & inibidores
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/metabolismo
Nitrocompostos/química
Relação Estrutura-Atividade
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase 2 Inhibitors); 0 (Indazoles); 0 (Lipopolysaccharides); 0 (Nitro Compounds); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.2174/1568026618666180119125255


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[PMID]:28454543
[Au] Autor:Subramanian S; Pallati PK; Sharma P; Agrawal DK; Nandipati KC
[Ad] Endereço:Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, USA.
[Ti] Título:TREM-1 associated macrophage polarization plays a significant role in inducing insulin resistance in obese population.
[So] Source:J Transl Med;15(1):85, 2017 Apr 28.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: TREM-1 acts as an amplifier of inflammation expressed on macrophages. The objective of this study was to evaluate the relationship between TREM-1 and macrophage polarization, and association of TREM-1 and M1 macrophage polarization with insulin resistance (IR) in obese population compared to non-obese population. METHODS: We enrolled 38 patients after obtaining IRB approval for this study. We evaluated the mRNA and protein expression levels of general macrophage marker (CD68), M1 marker (CD86, CCR7, iNOS, IFNγ, TNF-α and IL-6,), M2 marker (CD206, CD163, IL-10, IL-4) and chemokine axis (MCP-1, CCR2 and CCR5) along with TREM-1 and TREM-2 in omentum fat, subcutaneous fat, and liver biopsy tissues of non-obese (N = 5), obese non-diabetics, (N = 16) and obese diabetics (N = 17). RESULTS: The results of our study showed over-expression of TREM-1, M1 markers and down-regulation of TREM-2 and M2 markers in the omentum, subcutaneous and liver biopsies of obese patients (diabetics and non-diabetics) compared to non-obese patients. Overall, the obese diabetic group showed a significant (p < 0.05) higher number of patients with over expression of M1 markers (TREM-1, CD68, CD86, CCR-7, iNOS, IFN-γ, TNF-α, IL-6, MCP-1, CCR-2 and CCR-5) and down-regulation of M2 markers (CD206, CD163 and IL-4) in liver biopsy compared to obese non-diabetics. CONCLUSIONS: TREM-1 expression is significantly increased along with the M1 markers in liver biopsy of obese diabetic (17/17) and obese non-diabetic patients (9/16). Our data suggests that TREM-1 overexpression and M1 macrophage polarization are associated with obesity-induced IR.
[Mh] Termos MeSH primário: Polaridade Celular
Resistência à Insulina
Macrófagos/patologia
Obesidade/patologia
Receptor Gatilho 1 Expresso em Células Mieloides/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Biomarcadores/metabolismo
Biópsia
Comorbidade
Citocinas/metabolismo
Demografia
Diabetes Mellitus/genética
Diabetes Mellitus/patologia
Feminino
Fluorescência
Seres Humanos
Fígado/patologia
Masculino
Meia-Idade
Óxido Nítrico Sintase Tipo II/metabolismo
Obesidade/genética
Omento/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Quimiocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (Cytokines); 0 (RNA, Messenger); 0 (Receptors, Chemokine); 0 (TREM1 protein, human); 0 (Triggering Receptor Expressed on Myeloid Cells-1); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[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:170430
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1187-7


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[PMID]:28463694
[Au] Autor:Liu L; Yi H; He H; Pan H; Cai L; Ma Y
[Ad] Endereço:Key Lab of Health Informatics of Chinese Academy of Sciences, Guangdong Key Laboratory of Nanomedicine, Shenzhen Institutes of Advanced Technology, Chinese Academy of Science, Shenzhen 518055, PR China.
[Ti] Título:Tumor associated macrophage-targeted microRNA delivery with dual-responsive polypeptide nanovectors for anti-cancer therapy.
[So] Source:Biomaterials;134:166-179, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Repolarizing Tumor-associated macrophages (TAMs) to anti-tumor M1 macrophages with microRNA (miR) is a plausible approach for cancer treatment. However, how to achieve TAM-targeted miR delivery remains a challenge. The present study generated redox/pH dual-responsive hybrid polypeptide nanovectors, which consisted of self-crosslinked redox-responsive nanoparticles based on galactose-functionalized n-butylamine-poly(l-lysine)-b-poly(l-cysteine) polypeptides (GLC) coated with DCA-grafted sheddable PEG-PLL (sPEG) copolymers. The ex vivo study showed that sPEG shielded cationic GLC core at physiological pH but quickly shed off to re-expose GLC due to it charge reversible property. Encapsulation with sPEG/GLC nanovectors effectively facilitated macrophage-targeted miR delivery at the acidic condition but diminished miR uptake at neutral pH. Administration of miR155-loaded sPEG/GLC (sPEG/GLC/155) nanocomplexes increased miR155 expression in TAMs about 100-400 folds both in vitro and in vivo. sPEG/GLC/155 also effectively repolarized immunosuppressive TAMs to anti-tumor M1 macrophages through elevating M1 macrophage markers (IL-12, iNOS, MHC II) and suppressing M2 macrophage markers (Msr2 and Arg1) in TAMs. Moreover, the treatment of sPEG/GLC/155 significantly increased activated T lymphocytes and NK cells in tumors, which consequently led to robust tumor regression. Hence, TAM-targeted delivery of miR with redox/pH dual-responsive sPEG/GLC nanovectors could be a promising approach to re-polarize TAMs to M1 macrophages in situ and induce tumor regression.
[Mh] Termos MeSH primário: MicroRNAs/genética
Nanopartículas/química
Peptídeos/química
[Mh] Termos MeSH secundário: Animais
Eletroforese em Gel de Ágar
Feminino
Interleucina-12/metabolismo
Células Matadoras Naturais/metabolismo
Espectroscopia de Ressonância Magnética
Melanoma/metabolismo
Melanoma/terapia
Melanoma Experimental
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Nus
MicroRNAs/fisiologia
Óxido Nítrico Sintase Tipo II/metabolismo
Células RAW 264.7
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Peptides); 187348-17-0 (Interleukin-12); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:27779493
[Au] Autor:Sales AJ; Hiroaki-Sato VA; Joca SR
[Ad] Endereço:aDepartment of Pharmacology, School of Medicine of Ribeirão Preto bDepartment of Physics and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto cCenter for Interdisciplinary Research on Applied Neurosciences (NAPNA), University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
[Ti] Título:Participation of hippocampal nitric oxide synthase and soluble guanylate cyclase in the modulation of behavioral responses elicited by the rat forced swimming test.
[So] Source:Behav Pharmacol;28(1):19-29, 2017 02.
[Is] ISSN:1473-5849
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Systemic or hippocampal administration of nitric oxide (NO) synthase inhibitors induces antidepressant-like effects in animals, implicating increased hippocampal levels of NO in the neurobiology of depression. However, the role played by different NO synthase in this process has not been clearly defined. As stress is able to induce neuroinflammatory mechanisms and trigger the expression of inducible nitric oxide synthase (iNOS) in the brain, as well as upregulate neuronal nitric oxide synthase (nNOS) activity, the aim of the present study was to investigate the possible differential contribution of hippocampal iNOS and nNOS in the modulation of the consequences of stress elicited by the forced swimming test. Male Wistar rats received intrahippocampal injections, immediately after the pretest or 1 h before the forced swimming test, of selective inhibitors of nNOS (N-propyl-L-arginine), iNOS (1400W), or sGC (ODQ), the main pharmacological target for NO. Stress exposure increased nNOS and phospho-nNOS levels at all time points, whereas iNOS expression was increased only 24 h after the pretest. All drugs induced an antidepressant-like effect. However, whereas the nNOS inhibitor was equally effective when injected at different times, the iNOS inhibitor was more effective 24 h after the pretest. These results suggest that hippocampal nNOS and iNOS contribute to increase in NO levels in response to stress, although with a differential time course after stress exposure.
[Mh] Termos MeSH primário: Óxido Nítrico Sintase Tipo II/metabolismo
Óxido Nítrico Sintase Tipo I/metabolismo
Guanilil Ciclase Solúvel/metabolismo
Estresse Psicológico/metabolismo
[Mh] Termos MeSH secundário: Amidinas/farmacologia
Animais
Arginina/análogos & derivados
Arginina/farmacologia
Benzilaminas/farmacologia
Modelos Animais de Doenças
Hipocampo/metabolismo
Masculino
Óxido Nítrico/metabolismo
Oxidiazóis/farmacologia
Ratos
Ratos Wistar
Natação
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1H-(1,2,4)oxadiazolo(4,3-a)-quiloxalin-1-one); 0 (Amidines); 0 (Benzylamines); 0 (N(omega)-propylarginine); 0 (N-(3-(aminomethyl)benzyl)acetamidine); 0 (Oxadiazoles); 31C4KY9ESH (Nitric Oxide); 94ZLA3W45F (Arginine); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 4.6.1.2 (Soluble Guanylyl Cyclase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1097/FBP.0000000000000263


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[PMID]:28456769
[Au] Autor:Al Dera H
[Ad] Endereço:Department of Basic Medical Sciences, College of Medicine at King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Kingdom of Saudi Arabia. derah@ksau-hs.edu.sa.
[Ti] Título:Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta.
[So] Source:J Physiol Pharmacol;68(1):47-56, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study was carried out to investigate the expression pattern and role of osteopontin (OPN) in late global ischemia-reperfusion (I/R) injury with or without resveratrol (RES) pre-treatment. Young male rats were divided into 3 groups (n = 12) of I) sham, II) I/R model group and III) I/R + RES. Vehicle and RES (20 mg/kg) were administered to designed groups intraperitoneally 30 days prior global I/R injury (2-VO) induction and continued for 7 days, later. Then, percentages of infarct areas, mRNA levels of OPN, inducible nitric oxide synthase (iNOS) and other biochemical parameter related to endogenous antioxidants activities and inflammation were measured in the cerebral cortices of all groups. Significant elevations in the levels of malondialdehyde (MDA), the inflammatory mediator interleukin 1ß (IL-1ß), chemokines (KC and MIP-2) and adhesive molecules (ICAM-1) as well as parallel reductions in enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and chloramphenicol acetyltransferase (CAT) were observed in the cerebral homogenates of rats with late I/R injury. Associated with these changes, mRNA levels of OPN were significantly downregulated and those of iNOS and Bax were upregulated. All these changes were reversed by in 2-VO I/R induced rats pre-administered RES. These findings suggest that inhibition of sustained inflammatory response driven by IL-1ß, decreased activities of endogenous antioxidants and downregulation of OPN induced upregulation of iNOS play important roles in the pathogenesis of neurodegeneration during late cerebral I/R injury, effects that can be modulated by RES which might explain its neuroprotection effect during late global ischemia.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/tratamento farmacológico
Catalase/metabolismo
Córtex Cerebral/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocinas/metabolismo
Glutationa Peroxidase/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/metabolismo
Masculino
Fármacos Neuroprotetores/uso terapêutico
Óxido Nítrico Sintase Tipo II/genética
Osteopontina/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
Traumatismo por Reperfusão/tratamento farmacológico
Estilbenos/uso terapêutico
Superóxido Dismutase/metabolismo
Regulação para Cima
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (Cxcl2 protein, rat); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Neuroprotective Agents); 0 (Spp1 protein, rat); 0 (Stilbenes); 0 (bcl-2-Associated X Protein); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 147037-79-4 (keratinocyte-derived chemokines); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.15.1.1 (Superoxide Dismutase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28456767
[Au] Autor:Almeida RT; Galdino G; Perez AC; Silva G; Romero TR; Duarte ID
[Ad] Endereço:Department of Pharmacology, Institute of Biological Sciences, Federal University of Belo Horizonte, Minas Gerais, Brazil. imitri@icb.ufmg.br.
[Ti] Título:St36 electroacupuncture activates nNOS, iNOS and ATP-sensitive potassium channels to promote orofacial antinociception in rats.
[So] Source:J Physiol Pharmacol;68(1):27-33, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Orofacial pain is pain perceived in the face and/or oral cavity, generally caused by diseases or disorders of regional structures, by dysfunction of the nervous system, or through referral from distant sources. Treatment of orofacial pain is mainly pharmacological, but it has increased the number of reports demonstrating great clinical results with the use of non-pharmacological therapies, among them electroacupuncture. However, the mechanisms involved in the electroacupuncture are not well elucidated. Thus, the present study investigate the involvement of the nitric oxide synthase (NOS) and ATP sensitive K channels (KATP) in the antinociception induced by electroacupuncture (EA) at acupoint St36. Thermal nociception was applied in the vibrissae region of rats, and latency time for face withdrawal was measured. Electrical stimulation of acupoint St36 for 20 minutes reversed the thermal withdrawal latency and this effect was maintained for 150 min. Intraperitoneal administration of specific inhibitors of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and a KATP channels blocker reversed the antinociception induced by EA. Furthermore, nitrite concentration in cerebrospinal fluid (CSF) and plasma, increased 4 and 3-fold higher, respectively, after EA. This study suggests that NO participates of antinociception induced by EA by nNOS, iNOS and ATP-sensitive K channels activation.
[Mh] Termos MeSH primário: Pontos de Acupuntura
Eletroacupuntura
Dor Facial/terapia
Manejo da Dor
[Mh] Termos MeSH secundário: Animais
Dor Facial/fisiopatologia
Temperatura Alta/efeitos adversos
Canais KATP/antagonistas & inibidores
Canais KATP/fisiologia
Masculino
Óxido Nítrico Sintase Tipo I/antagonistas & inibidores
Óxido Nítrico Sintase Tipo I/fisiologia
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/fisiologia
Nitritos/sangue
Nitritos/líquido cefalorraquidiano
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KATP Channels); 0 (Nitrites); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29307523
[Au] Autor:Wu GJ; Lin YW; Chuang CY; Tsai HC; Chen RM
[Ad] Endereço:Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan; Department of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:Liver nitrosation and inflammation in septic rats were suppressed by propofol via downregulating TLR4/NF-κB-mediated iNOS and IL-6 gene expressions.
[So] Source:Life Sci;195:25-32, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Propofol can be applied as an anesthetic or sedative agent for septic patients. Our previous studies showed that propofol ameliorated inflammation- and nitrosative stress-induced cellular insults. This study further evaluated effects of propofol on cecal ligation and puncture (CLP)-induced septic insults to rats and its possible mechanisms. MAIN METHODS: Wistar rats were administered with CLP and effects of propofol on CLP-induced liver dysfunction and rat death were evaluated. Levels of hepatic or systemic nitrogen oxides (NOx) and interleukin (IL)-6 were quantified. Sequentially, inducible nitric oxide synthase (iNOS) and IL-6 gene expressions, toll-like receptor 4 (TLR4) protein levels, and nuclear factor (NF)-κB translocation were determined. KEY FINDINGS: Subjecting rats to CLP led to body weight loss, liver weight gain, and death. Administration of propofol lessened CLP-induced augmentations of serum and hepatic nitrosative stress and IL-6 levels. Additionally, propofol suppressed CLP-induced enhancements in levels of hepatic iNOS protein. Furthermore, the CLP-induced iNOS and IL-6 mRNA expressions in the liver were inhibited following propofol administration. Sequentially, subjecting rats to CLP enhanced hepatic TLR4 protein levels and NF-κB translocation to nuclei, but propofol inhibited these augmentations. SIGNIFICANCE: Consequently, exposure to propofol protected against CLP-induced liver dysfunction and increased the survival rates of the animals. This study shows that propofol can protect rats against septic insults through suppression of systemic and hepatic nitrosative and inflammatory stress due to inhibition of TLR4/NF-κB-mediated iNOS and IL-6 mRNA and protein expressions.
[Mh] Termos MeSH primário: Hepatite/tratamento farmacológico
Hipnóticos e Sedativos/uso terapêutico
Interleucina-6/biossíntese
Fígado/metabolismo
Fígado/patologia
NF-kappa B/efeitos dos fármacos
Óxido Nítrico Sintase Tipo II/biossíntese
Nitrosação/efeitos dos fármacos
Propofol/uso terapêutico
Sepse/tratamento farmacológico
Receptor 4 Toll-Like/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Doenças do Ceco/metabolismo
Doenças do Ceco/patologia
Regulação para Baixo
Regulação da Expressão Gênica/efeitos dos fármacos
Hepatite/metabolismo
Hepatite/patologia
Interleucina-6/genética
Masculino
Óxido Nítrico Sintase Tipo II/genética
Ratos
Ratos Wistar
Sepse/metabolismo
Sepse/patologia
Translocação Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Hypnotics and Sedatives); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); YI7VU623SF (Propofol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:28464218
[Au] Autor:Köstlin N; Vogelmann M; Spring B; Schwarz J; Feucht J; Härtel C; Orlikowsky TW; Poets CF; Gille C
[Ad] Endereço:Department of Neonatology, Tübingen University Children's Hospital, Tübingen, Germany.
[Ti] Título:Granulocytic myeloid-derived suppressor cells from human cord blood modulate T-helper cell response towards an anti-inflammatory phenotype.
[So] Source:Immunology;152(1):89-101, 2017 09.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Infections are a leading cause of perinatal morbidity and mortality. The outstandingly high susceptibility to infections early in life is mainly attributable to the compromised state of the neonatal immune system. One important difference to the adult immune system is a bias towards T helper type 2 (Th2) responses in newborns. However, mechanisms regulating neonatal T-cell responses are incompletely understood. Granulocytic myeloid-derived suppressor cells (GR-MDSC) are myeloid cells with a granulocytic phenotype that suppress various functions of other immune cells and accumulate under physiological conditions during pregnancy in maternal and fetal blood. Although it has been hypothesized that GR-MDSC accumulation during fetal life could be important for the maintenance of maternal-fetal tolerance, the influence of GR-MDSC on the immunological phenotype of neonates is still unclear. Here, we investigated the impact of GR-MDSC isolated from cord blood (CB-MDSC) on the polarization of Th cells. We demonstrate that CB-MDSC inhibit Th1 responses and induced Th2 responses and regulatory T (Treg) cells. Th1 inhibition was cell-contact dependent and occurred independent of other cell types, while Th2 induction was mediated independently of cell contact through expression of ArgI and reactive oxygen species by CB-MDSC and partially needed the presence of monocytes. Treg cell induction by CB-MDSC also occurred cell-contact independently but was partially mediated through inducible nitric oxide synthase. These results point towards a role of MDSC in regulating neonatal immune responses. Targeting MDSC function in neonates could be a therapeutic opportunity to improve neonatal host defence.
[Mh] Termos MeSH primário: Plasticidade Celular
Sangue Fetal/imunologia
Granulócitos/imunologia
Inflamação/prevenção & controle
Células Supressoras Mieloides/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Arginase/imunologia
Arginase/metabolismo
Comunicação Celular
Células Cultivadas
Técnicas de Cocultura
Sangue Fetal/citologia
Granulócitos/metabolismo
Seres Humanos
Recém-Nascido
Inflamação/imunologia
Inflamação/metabolismo
Células Supressoras Mieloides/metabolismo
Óxido Nítrico Sintase Tipo II/imunologia
Óxido Nítrico Sintase Tipo II/metabolismo
Fenótipo
Espécies Reativas de Oxigênio/imunologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Células Th1/imunologia
Células Th1/metabolismo
Células Th2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12751


  9 / 18848 MEDLINE  
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Baracat, Emílio Carlos Elias
Tresoldi, Antonia Teresinha
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[PMID]:29253610
[Au] Autor:Alvarez AE; Marson FAL; Bertuzzo CS; Bastos JCS; Baracat ECE; Brandão MB; Tresoldi AT; das Neves Romaneli MT; Almeida CCB; de Oliveira T; Schlodtmann PG; Corrêa E; de Miranda MLF; Dos Reis MC; De Pieri JV; Arns CW; Ribeiro JD
[Ad] Endereço:Department of Pediatrics, Faculty of Medical Sciences, University of Campinas, Rua Tessália Vieira de Camargo, 126, Cidade Universitária Zeferino Vaz, Campinas CEP 13083-887, São Paulo, Brazil. Electronic address: alfonso@cepap.med.br.
[Ti] Título:Association between single nucleotide polymorphisms in TLR4, TLR2, TLR9, VDR, NOS2 and CCL5 genes with acute viral bronchiolitis.
[So] Source:Gene;645:7-17, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute viral bronchiolitis is the leading cause of hospitalization among infants during the first year of life. Most infants hospitalized for bronchiolitis do not present risk factors and are otherwise healthy. Our objective was to determine the genetic features associated with the risk and a severe course of bronchiolitis. METHODS: We prospectively evaluated 181 infants with severe bronchiolitis admitted at three hospitals over a 2-year period, who required oxygen therapy. The control group consisted of 536 healthy adults. Patients were evaluated for the presence of comorbidities (premature birth, chronic respiratory disease, and congenital heart disease), underwent nasopharyngeal aspirate testing for virus detection by multiplex-PCR, and SNPs identification in immune response genes. Patient outcomes were assessed. RESULTS: We observed association between SNP rs2107538*CCL5 and bronchiolitis caused by respiratory syncytial virus(RSV) and RSV-subtype-A, and between rs1060826*NOS2 and bronchiolitis caused by rhinovirus. SNPs rs4986790*TLR4, rs1898830*TLR2, and rs2228570*VDR were associated with progression to death. SNP rs7656411*TLR2 was associated with length of oxygen use; SNPs rs352162*TLR9, rs187084*TLR9, and rs2280788*CCL5 were associated with requirement for intensive care unit admission; while SNPs rs1927911*TLR4, rs352162*TLR9, and rs2107538*CCL5 were associated with the need for mechanical ventilation. CONCLUSIONS: Our findings provide some evidence that SNPs in CCL5 and NOS2 are associated with presence of bronchiolitis and SNPs in TLR4, TLR2, TLR9, VDR and CCL5 are associated with severity of bronchiolitis.
[Mh] Termos MeSH primário: Bronquiolite Viral/genética
Quimiocina CCL5/genética
Óxido Nítrico Sintase Tipo II/genética
Polimorfismo de Nucleotídeo Único
Receptores de Calcitriol/genética
Receptores Toll-Like/genética
[Mh] Termos MeSH secundário: Bronquiolite Viral/virologia
Progressão da Doença
Feminino
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Lactente
Recém-Nascido
Masculino
Nasofaringe/virologia
Estudos Retrospectivos
Receptor 2 Toll-Like/genética
Receptor 4 Toll-Like/genética
Receptor Toll-Like 9/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Receptors, Calcitriol); 0 (TLR2 protein, human); 0 (TLR4 protein, human); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Toll-Like Receptor 9); 0 (Toll-Like Receptors); 0 (VDR protein, human); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


  10 / 18848 MEDLINE  
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[PMID]:28747341
[Au] Autor:Suwanpradid J; Shih M; Pontius L; Yang B; Birukova A; Guttman-Yassky E; Corcoran DL; Que LG; Tighe RM; MacLeod AS
[Ad] Endereço:Department of Dermatology, Duke University, Durham, NC 27710.
[Ti] Título:Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.
[So] Source:J Immunol;199(5):1827-1834, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The innate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined. Using human skin from contact dermatitis patients and a mouse model of CHS, we find that hapten allergens disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MΦ), which renders those cells ineffectual in suppressing skin inflammation. Mice lacking Arg1 in MΦ develop increased CHS characterized by elevated ear thickening, mono/MΦ-dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice. Treatment of Arg1 ; LysMCre mice with a selective NOS inhibitor or knockout of , encoding iNOS, significantly ameliorates CHS. Our findings suggest a critical role for Arg1 in mono/MΦ in suppressing CHS through dampening expression. These results support that increasing Arg1 may be a potential therapeutic avenue in treating allergic contact dermatitis.
[Mh] Termos MeSH primário: Arginase/metabolismo
Dermatite Alérgica de Contato/imunologia
Macrófagos/imunologia
Óxido Nítrico Sintase Tipo II/metabolismo
Pele/imunologia
[Mh] Termos MeSH secundário: Alérgenos/imunologia
Animais
Arginase/genética
Células Cultivadas
Dermatite Alérgica de Contato/genética
Modelos Animais de Doenças
Feminino
Haptenos/imunologia
Seres Humanos
Imunidade Inata
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Óxido Nítrico Sintase Tipo II/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Allergens); 0 (Haptens); 0 (Interleukin-6); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700739



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