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Decalepis hamiltonii Inhibits Tumor Progression and Metastasis by Regulating the Inflammatory Mediators and Nuclear Factor κB Subunits

机译:拟南芥(Decalepis hamiltonii)通过调节炎症介质和核因子κB亚基抑制肿瘤的进展和转移

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Metastasis is an extremely complex process that is a major problem in the management of cancer. In the present study, we had evaluated the antimetastatic activity of Decalepis hamiltonii using B16F-10 melanoma-induced experimental lung metastasis in a C57BL/6 mice model. D hamiltonii treatment significantly (P D hamiltonii treatment. The levels of proinflammatory cytokines such as tumor necrosis factor α, interleukin (IL)-1β, IL-6, granulocyte monocyte colony-stimulating factor, and IL-2 in the serum of these animals were significantly altered after D hamiltonii treatment. The serum NO level was also found to be significantly decreased after D hamiltonii treatment. This decreased NO level after D hamiltonii treatment was also accompanied by decreased inducible NO synthase and cyclooxygenase-2 expression. The study reveals that D hamiltonii treatment could alter proinflammatory cytokine production and could inhibit the activation and nuclear translocation of p65 and p50 subunits of nuclear factor κB in B16F-10 cells.
机译:转移是一个极其复杂的过程,是癌症治疗中的主要问题。在本研究中,我们使用B16F-10黑色素瘤诱导的C57BL / 6小鼠模型的实验性肺转移,评估了十足夜蛾的抗转移活性。这些动物的血清中的D汉密尔顿治疗显着(PD汉密尔顿治疗。肿瘤坏死因子α,白介素(IL)-1β,IL-6,粒细胞单核细胞集落刺激因子和IL-2等促炎细胞因子的水平分别为D汉密尔顿处理后血清NO水平明显降低; D汉密尔顿处理后血清NO水平也明显降低; D汉密尔顿处理后血清NO水平降低,同时诱导型NO合酶和环氧合酶2表达降低。汉密尔顿处理可以改变促炎细胞因子的产生,并可以抑制B16F-10细胞中核因子κB的p65和p50亚基的激活和核易位。

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