Decalepis hamiltonii inhibits tumor progression and metastasis by regulating the inflammatory mediators and nuclear factor κB subunits.

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 HAMILTONI: using B16F-10 melanoma-induced experimental lung metastasis in a C57BL/6 mice model.

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treatment significantly ( : < .01) inhibited lung tumor nodule formation and reduced the lung collagen hydroxyproline, hexosamine, and uronic acid levels. Similarly serum sialic acid and γ-glutamyl transpeptidase levels were also significantly inhibited after

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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

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treatment. The serum NO level was also found to be significantly decreased after

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treatment. This decreased NO level after

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treatment was also accompanied by decreased inducible NO synthase and cyclooxygenase-2 expression. The study reveals that

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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.