Inhibitory Effects of Astaxanthin on LPS-Induced Raw 264.7 Inflammation and Breast Cancer McF-7 Cell Lines Proliferation

Astaxanthin (ASTA) is a xanthophyll carotenoid pigment derived from bacteria, yeasts, and microalgae Hematococcus pluvialis and is known to exhibit a potent antioxidant activity that protects the biological system against free radicals. Moreover, ASTA is also known to possess medicinal values such as anti-cancer and anti-inflammatory activities, however, the mechanism on how ASTA exhibits these properties are not well understood. The aims of this study were to elucidate the mechanism of the cytotoxic effect of ASTA on breast cancer cell line MCF-7 and its anti-inflammatory effect on monocytic RAW 264.7 cells. Cytotoxic activity of ASTA on both cells line was determined using MTT assays and further studied the anti-cancer mechanism of ASTA on MCF-7 by computational docking study. Meanwhile, the anti-inflammatory activity mechanism was elucidated on LPS induced nitric oxide (NO) production and its association with cell activation. Results revealed that ASTA had a different cytotoxic effect on breast cancer cell MCF-7 and RAW 264.7 cells. In addition, the computational docking study revealed that the anti-cancer activity of ASTA was due to significant high energy efficiency combining with estrogen receptor (-8.3) and Quinon reductase (-8.1) rather than the Janus kinase receptor (-7.4). We also demonstrated the ability of ASTA to inhibit the LPS-induced RAW 264.7 to become activated macrophages and subsequently reduced the nitric oxide production. In conclusion, ASTA exhibits its anti-inflammatory activities by affecting macrophages activation in vitro. Meanwhile, ASTA also has been demonstrated to have anti-proliferative activity by significantly reducing the MCF-7 cell viability and survivability. Computational molecular docking further revealed the anti-proliferative mechanism of ASTA, where it has a strong affinity towards ER and Quinone reductase receptors on MCF-7 but not JNK2.