Anti‐inflammatory effects of CoQ10 and colorless carotenoids

Abstract

CoQ10 (ubiquinone, coenzyme Q10) and carotenoids are popular antioxidants used in many skin care products to protect the skin from free radical damage. To evaluate the effects of CoQ10 and colorless carotenoids on the production of inflammatory mediators in human dermal fibroblasts treated with UV radiation (UVR) and to investigate the possible synergistic effects of these two antioxidants. Normal human dermal fibroblast cell cultures were exposed to either 50 mJ of UVR or to IL-1 and then incubated with various concentrations of either CoQ10, the colorless carotenoids, phytoene and phytofluene, or to combinations of these antioxidants. After 24 h in culture, cells and spent medium were harvested and assayed by enzyme-linked immunosorbent assay for prostaglandin E2 (PGE-2), interleukin 6 (IL-6), and matrix metalloproteinase 1 (MMP-1). In addition, the ability of the carotenoids to protect CoQ10 from oxidation by the reactive oxygen species (ROS), hyperchlorite, was also determined. Human fibroblasts respond to UVR or to IL-1 by increasing the production of various inflammatory mediators including PGE-2, IL-1, and IL-6 and proteases such as collagenase (MMP-1). Treatment of fibroblasts with 10 microm of CoQ10 suppressed the UVR- or IL-1-induced increase in PGE-2, IL-6, and MMP-1. The combination of carotenoids and CoQ10 produced an enhanced inhibition of these three inflammatory mediators. Furthermore, the colorless carotenoids, phytoene and phytofluene, protected CoQ10 from degradation by the ROS, hypochlorite. CoQ10 is able to suppress the UVR- or IL-1-induced inflammatory response in dermal fibroblasts. Furthermore, this compound can block the UVR induction of the matrix-eroding enzyme, MMP-1. Finally, the combination of carotenoids plus CoQ10 results in enhanced suppression of inflammation. The results suggest that the combination of carotenoids and CoQ10 in topical skin care products may provide enhanced protection from inflammation and premature aging caused by sun exposure.