Decalepis hamiltonii Inhibits Tumor Progression and Metastasis by Regulating the Inflammatory Mediators and Nuclear Factor {kappa}B 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 hamiltonii using B16F-10 melanoma-induced experimental lung metastasis in a C57BL/6 mice model. D hamiltonii treatment significantly (P < .01) inhibited lung tumor nodule formation and reduced the lung collagen hydroxyproline, hexosamine, and uronic acid levels. Similarly serum sialic acid and -glutamyl transpeptidase levels were also significantly inhibited after 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 B in B16F-10 cells.
Source: Integrative Cancer Therapies - Category: Cancer & Oncology Authors: Tags: Articles Source Type: research