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

Abstract

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. 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 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 treatment. The serum NO level was also found to be significantly decreased after treatment. This decreased NO level after treatment was also accompanied by decreased inducible NO synthase and cyclooxygenase-2 expression. The study reveals that 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.