Modulação por PGE Ind.3 no perfil de subpopulações celulares e citocinas na evolução do Tumor Ascítico de Ehrlich (TAE)
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Data
2001
Autores
Gentile, Luciana Boffoni [UNESP]
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
O presente trabalho objetivou avaliar o envolvimento das prostaglandinas no crescimento tumoral, influxo inflamatório e secreação de citocinas durante a evolução do Tumor Ascítico de Ehrlich (TAE). Para tanto, camundongos foram inoculados com 1 x 103 células tumorais (ip) e tratados com indometacina (1mg/Kg,1x/dia,ip) ou com diluente (0,1 ml,1x/dia,ip). Decorridos 1, 3, 6, 10 e 13 dias os animais foram sacrificados e avaliados quanto ao influxo inflamatório diferencial, secreção de TNF-a, IL1-a, IL-2, IL- 4, IL-6, IL-10 e IL-13 e níveis de PGE2 no lavado peritoneal.. Dois grupos controle adicionais foram constituídos de animais não portadores de TAE tratados com indometacina ou diluente, seguindo o mesmo protocolo. Os resultados obtidos demonstraram que o implante do TAE induz produção de PGE2 durante toda sua evolução; aumento do número de células neoplásicas a partir do 10o dia e diminuição do influxo de células mesoteliais no 10º dia e de basófilos no 10º e 13º dia pós implante neoplásico. Em relação as citocinas o TAE induziu produção de IL-6 no 10º e 13º dia e de IL 2 no 13º dia, não alterando de modo significativo o perfil das outras citocinas estudadas. O tratamento de animais portadores de TAE com indometacina, foi eficaz em inibir o crescimento tumoral e a síntese de PGE2 a partir do 10o dia de crescimento neopásico, e promoveu aumento significativo no influxo de neutrófilos segmentados e de células nucleadas, apenas em tempos iniciais da evolução tumoral. Ainda, o tratamento com indometacina promoveu síntese de IL-13 e inibição significativa de IL-6 no 13o dia de crescimento tumoral, não alterando as outras citocinas analisadas. No grupo não portador de tumor tratado com indometacina observamos aumento no influxo de neutrófilos segmentados no 1º dia... .
The aim of the present study was investigate the prostaglandin involvement during the growth of Ehrlich Ascites Tumor (EAT), using as parameters: tumoral growth, inflammatory influx and cytokine profile. Mice were inoculated with 1 x 103 tumor cells (ip) and treated with indomehacin (1mg/Kg,1x/day,ip) or diluent (0,1ml,1x/day,ip). After 1, 3, 6, 10 and 13 days the animals were sacrificed and evaluated in relation to inflammatory influx, secretion of TNF -a , IL1-a, IL-2, IL-4, IL-6, IL-10 and IL-13 and PGE2 level, in peritoneal cavity. Two groups no bearing EAT were treated with indomethacina or diluent as control ,following the same protocol. The results demonstrated that EAT implant induces PGE2 production during all evolution; increases tumoral cells number from the 10th day and decreases the mesotelial cells on 10th day and basophils cells on 10th and 13rd day.The cytokine profile showed EAT induces production of IL 6 from 10th day and of IL 2 on 13rd day, the other studied cytokines were not affected in a significant way. The indomethacin treatment of EAT bearing mice inhibited the tumoral growth and PGE2 synthesis from the 10th day and promoted significant increase on the neutrophils influx and total inflammatory cells, just in initial times of the tumoral evolution. Indomethacin treatment also promoted IL-13 synthesis and significant inhibition of IL-6 on 13rd day of EAT growth, but did not altered the others cytokines. The indomethacin treatment of animals do not bearing EAT increases neutrophils influx on the 1st day, lymphocytes on the 3rd day, eosinophils on 10th day; and no detected alteration was detected on cytokine profile Taken together, the results suggest that EAT growth is modulate by PGE2 and the inhibition of the tumoral growth could be partly related with suppression of IL-6 and liberation of IL-13.
The aim of the present study was investigate the prostaglandin involvement during the growth of Ehrlich Ascites Tumor (EAT), using as parameters: tumoral growth, inflammatory influx and cytokine profile. Mice were inoculated with 1 x 103 tumor cells (ip) and treated with indomehacin (1mg/Kg,1x/day,ip) or diluent (0,1ml,1x/day,ip). After 1, 3, 6, 10 and 13 days the animals were sacrificed and evaluated in relation to inflammatory influx, secretion of TNF -a , IL1-a, IL-2, IL-4, IL-6, IL-10 and IL-13 and PGE2 level, in peritoneal cavity. Two groups no bearing EAT were treated with indomethacina or diluent as control ,following the same protocol. The results demonstrated that EAT implant induces PGE2 production during all evolution; increases tumoral cells number from the 10th day and decreases the mesotelial cells on 10th day and basophils cells on 10th and 13rd day.The cytokine profile showed EAT induces production of IL 6 from 10th day and of IL 2 on 13rd day, the other studied cytokines were not affected in a significant way. The indomethacin treatment of EAT bearing mice inhibited the tumoral growth and PGE2 synthesis from the 10th day and promoted significant increase on the neutrophils influx and total inflammatory cells, just in initial times of the tumoral evolution. Indomethacin treatment also promoted IL-13 synthesis and significant inhibition of IL-6 on 13rd day of EAT growth, but did not altered the others cytokines. The indomethacin treatment of animals do not bearing EAT increases neutrophils influx on the 1st day, lymphocytes on the 3rd day, eosinophils on 10th day; and no detected alteration was detected on cytokine profile Taken together, the results suggest that EAT growth is modulate by PGE2 and the inhibition of the tumoral growth could be partly related with suppression of IL-6 and liberation of IL-13.
Descrição
Palavras-chave
Tumores ascíticos - Aspectos imunológicos, Tumor Ascítico de Ehrlich (TAE), Ehrlich Ascites Tumor (EAT)
Como citar
GENTILE, Luciana Boffoni. Modulação por PGE Ind.3 no perfil de subpopulações celulares e citocinas na evolução do Tumor Ascítico de Ehrlich (TAE). 2001. 103 f. Dissertação (mestrado) - Universidade Estadual Paulista, Faculdade de Medicina de Botucatu, 2001.