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首页> 外文期刊>Mediators of inflammation >Modulation of Cytokines Production by Indomethacin Acute Dose during the Evolution of Ehrlich Ascites Tumor in Mice
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Modulation of Cytokines Production by Indomethacin Acute Dose during the Evolution of Ehrlich Ascites Tumor in Mice

机译:小鼠EHRLICH腹水肿瘤中吲哚美辛急性剂量的细胞因子产生的调节

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摘要

The aim of the present study was to investigate the influence of a nonselective COX1/COX2 inhibitor (indomethacin) on tumor growth of Ehrlich Ascites Tumor (EAT) in mice, using as parameters the tumor growth and cytokine profile. Mice were inoculated with EAT cells and treated with indomethacin. After 1, 3, 6, 10, and 13 days the animals were evaluated for the secretion of TNF alpha, IL-1 alpha, IL-2, IL-4, IL-6, IL-10, and IL-13 and PGE(2) level in peritoneal cavity. The results have shown that EAT induces PGE(2) production and increases tumor cells number from the 10th day. The cytokine profile showed EAT induces production of IL-6 from 10th day and of IL-2 on 13th day; the other studied cytokines were not affected in a significant way. The indomethacin treatment of EAT-bearing mice inhibited the tumor growth and PGE(2) synthesis from the 10th day. In addition, the treatment of EAT-bearing mice with indomethacin has stimulated the IL-13 production and has significantly inhibited IL-6 in the 13th day of tumor growth. Taken together, the results have demonstrated that EAT growth is modulated by PGE(2) and the inhibition of the tumor growth could be partly related to suppression of IL-6 and induction of IL-13.
机译:本研究的目的是研究非选择性COX1 / COX2抑制剂(吲哚美辛)对小鼠肿瘤肿瘤(吃)肿瘤生长的影响,用作肿瘤生长和细胞因子谱的参数。用食用细胞接种小鼠并用吲哚美辛处理。在1,3,6,10和13天后,评估动物的分泌TNFα,IL-1α,IL-2,IL-4,IL-6,IL-10和IL-13和PGE (2)腹膜腔水平。结果表明,吃诱导PGE(2)产生并增加第10天的肿瘤细胞数。细胞因子谱显示在第10天和IL-2中诱导IL-6的产生;另一种研究的细胞因子不受显着的影响。携带小鼠的吲哚美辛治疗抑制肿瘤生长和第10天的肿瘤生长和PGE(2)合成。此外,用吲哚美辛的食用小鼠治疗刺激了IL-13的生产,并在肿瘤生长的第13天具有显着抑制的IL-6。在一起,结果表明,通过PGE(2)调节吃生长,肿瘤生长的抑制可以部分地与IL-6的抑制和IL-13的诱导相关。

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