Anti-tumor mechanism of eicosapentaenoic acid (EPA) on ovarian tumor model by improving the immunomodulatory activity in F344 rats

[Display omitted] •EPA could attenuate ovarian cancer by improving the immunomodulatory.•EPA could increase the index of spleens and thymus and phagocytosis activity of macrophages.•The immunomodulatory effects of EPA were associated with PI3K/Akt, ERK1/2 and NF-κB P65 expression. Eicosapentaenoic acid (EPA) has been known to induce human ovarian cancer cells apoptosis in vitro. However, the anti-tumor mechanisms of EPA in vivo have been rarely reported. In this study, the effect of EPA on the ovarian cancer rat model and its related mechanism were investigated. The results showed after EPA treatment, the index of spleens and thymus was significantly increased, and the proliferation of spleen cells, the natural killer (NK) cell activity and phagocytosis activity of macrophages were prompted. Besides, EPA could reverse the decrease of CD4+ and CD8+ T lymphocytes induced by ovarian cancer. It was found that EPA could inhibit the phosphorylation status of PI3K (phosphatidylinositol 3-hydroxy kinase)/Akt (serine-threonine kinase), ERK1/2 (extracellular signal-regulated kinase 1/2) and NF-κB p65, and prompt the expression of cytochrome C and caspase-3. These results suggested that EPA has a remarkable anti-tumor activity by improving the immunomodulatory on the ovarian cancer rat model.