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1.
Cytokine ; 36(3-4): 123-33, 2006 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-17188888

RESUMO

Two variants of this Walker 256 tumor have been previously reported as Walker 256 A and variant AR. The variant A has more aggressive property than variant AR and can induce systemic effects such as anorexia, sodium and water retention, followed by weight loss and death. The mechanisms involved in enhancing tumor regression and progression in this model are still incompletely understood. In the present study, serum and spleen mononuclear cells and tumor cells from animals inoculated with variants A and AR, were isolated to investigate the TGF-beta, IL-12, IFN-gamma and TNF-alpha and relationship with anemia, weight of animals, weight of spleen, volume of tumor and osmotic fragility compared with controls inoculated with Ringer Lactate. Results demonstrate that the group inoculated with variant A, compared to variant AR, shows high levels of TGF-beta gene expression in both tumor tissue and spleen cells, no expression of IFN-gamma and a progressive and higher levels of IL-12 in tumor tissue without inflammatory infiltrate visualized by optical microscopy. These results suggest that the aggressively of variant A is relate to cytokine modulation, facilitating the growth and escape of tumor cells. Furthermore, IL-12 seems to be constitutively expressed in both tumor lineage A and AR.


Assuntos
Carcinoma 256 de Walker/genética , Citocinas/genética , Anemia/sangue , Anemia/genética , Anemia/patologia , Animais , Peso Corporal , Carcinoma 256 de Walker/sangue , Carcinoma 256 de Walker/patologia , Citocinas/sangue , Ensaio de Imunoadsorção Enzimática , Expressão Gênica , Hemoglobinas/análise , Interferon gama/sangue , Interferon gama/genética , Interleucina-12/genética , Masculino , Tamanho do Órgão , Fragilidade Osmótica , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Baço/metabolismo , Baço/patologia , Fator de Crescimento Transformador beta/sangue , Fator de Crescimento Transformador beta/genética , Fator de Necrose Tumoral alfa/genética
2.
Endocrinology ; 146(10): 4192-9, 2005 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-16002529

RESUMO

Obesity has reached epidemic proportions in several regions of the world. General changes in lifestyle, including consumption of fat-rich food, are among the most important factors leading to an unprecedented increase in the prevalence of this disease. Weight gain results from an imbalance between caloric intake and energy expenditure. Both of these parameters are under the tight control of specialized neurons of the hypothalamus that respond to peripheral anorexigenic and adipostatic signals carried by leptin and insulin. Here we show, by macroarray analysis, that high-fat feeding [hyperlipidic diet (HL)] induces the expression of several proinflammatory cytokines and inflammatory responsive proteins in hypothalamus. This phenomenon is accompanied by increased activation of c-Jun N-terminal kinase and nuclear factor-kappaB. In addition, HL feeding leads to impaired functional and molecular activation of the insulin-signaling pathway, which is paralleled by increased serine phosphorylation of the insulin receptor and insulin receptor substrate-2. Intracerebroventricular treatment of HL rats with a specific inhibitor of c-Jun N-terminal kinase (SP600125) restores insulin signaling and leads to a reduced caloric intake and weight loss. We conclude that HL feeding induces a local proinflammatory status in the hypothalamus, which results in impaired anorexigenic insulin signaling.


Assuntos
Gorduras na Dieta/efeitos adversos , Hipotálamo/fisiologia , Inflamação/fisiopatologia , Resistência à Insulina/fisiologia , Tecido Adiposo , Animais , Apetite/efeitos dos fármacos , Sequência de Bases , Primers do DNA , Ingestão de Energia/efeitos dos fármacos , Epididimo , Hipotálamo/efeitos dos fármacos , Inflamação/induzido quimicamente , Injeções Intraventriculares , Insulina/administração & dosagem , Insulina/farmacologia , Masculino , NF-kappa B/genética , Análise de Sequência com Séries de Oligonucleotídeos , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa
3.
Cytokine ; 26(4): 155-63, 2004 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-15149632

RESUMO

In experimental autoimmune encephalomyelitis, a classical model for multiple sclerosis, the cytokines provide the necessary signals to activate specific T cells for self-antigens. Gangliosides have multiple immunomodulatory activities, decreasing the lymphoproliferative responses and modulating cytokine production. Here, we tested the effects of gangliosides on the switching of Th1 to Th2 cytokine expression, in spleen cells obtained from Lewis rats during the acute phase of EAE, and after recovery from the disease. For this purpose, total RNA from spleen cells was isolated and submitted to RT-PCR to investigate Th1 (IL-2, TNF-alpha, and IFN-gamma) and Th2/Th3 (IL-10 and TGF-beta) cytokine gene expression. Results demonstrate that the group treated with gangliosides displays mild disease, with low expression of IFN-gamma mRNA and high TGF-beta mRNA expression. We conclude that the gangliosides may modulate Th1 cells by the synthesis of cytokines shifting the profile to the Th2/Th3 phenotype.


Assuntos
Encefalomielite Autoimune Experimental/imunologia , Gangliosídeos/imunologia , Células Th1/imunologia , Células Th2/imunologia , Animais , Sobrevivência Celular/imunologia , Sobrevivência Celular/fisiologia , Citocinas/genética , Citocinas/metabolismo , Encefalomielite Autoimune Experimental/fisiopatologia , Feminino , RNA Mensageiro/metabolismo , Ratos , Ratos Endogâmicos Lew , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Baço/metabolismo , Células Th1/metabolismo , Células Th2/metabolismo
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