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Modulation of Cytokines Production by Indomethacin Acute Dose during the Evolution of Ehrlich Ascites Tumor in Mice

机译:消炎痛急性小鼠演化过程中消炎痛急性剂量对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 TNFα, IL-1α, IL-2, IL-4, IL-6, IL-10, and IL-13 and PGE2 level in peritoneal cavity. The results have shown that EAT induces PGE2 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 PGE2 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 PGE2 and the inhibition of the tumor growth could be partly related to suppression of IL-6 and induction of IL-13.
机译:本研究的目的是使用肿瘤生长和细胞因子谱作为参数,研究非选择性COX1 / COX2抑制剂(吲哚美辛)对小鼠艾氏腹水肿瘤(EAT)肿瘤生长的影响。用EAT细胞接种小鼠并用消炎痛治疗。在1、3、6、10和13天后,评估动物的TNFα,IL-1α,IL-2,IL-4,IL-6,IL-10,IL-13和PGE2水平的分泌。腹腔。结果表明,从第10天开始,EAT会诱导PGE2的产生并增加肿瘤细胞的数量。细胞因子谱显示,EAT从第10天开始诱导IL-6的产生,在第13天诱导IL-2的产生。其他研究的细胞因子未受到重大影响。从第10天起,用消炎痛处理的EAT小鼠就抑制了肿瘤的生长和PGE2的合成。此外,用消炎痛治疗携带EAT的小鼠刺激了IL-13的产生,并在肿瘤生长的第13天显着抑制了IL-6。两者合计,结果表明EAT的生长受到PGE2的调节,并且肿瘤生长的抑制可能部分与IL-6的抑制和IL-13的诱导有关。

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