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.

二十碳五烯酸（EPA）已知可在体外诱导人卵巢癌细胞凋亡。然而，体内EPA的抗肿瘤机制鲜有报道。在这项研究中，研究了EPA对卵巢癌大鼠模型的影响及其相关机制。结果表明，经EPA处理后，脾，胸腺指数明显升高，提示脾细胞增殖，自然杀伤（NK）细胞活性和巨噬细胞吞噬活性。此外，EPA可以逆转卵巢癌引起的CD4 +和CD8 + T淋巴细胞的减少。发现EPA可以抑制PI3K（磷脂酰肌醇3-羟基激酶）/ Akt（丝氨酸-苏氨酸激酶），ERK1 / 2（细胞外信号调节激酶1/2）和NF-κBp65的磷酸化状态，并提示细胞色素C的表达和caspase-3。这些结果表明，EPA通过改善对卵巢癌大鼠模型的免疫调节作用而具有显着的抗肿瘤活性。