Naringin prevents ultraviolet-B radiation-induced oxidative damage and inflammation through activation of peroxisome proliferator-activated receptor γ in mouse embryonic fibroblast (NIH-3T3) cells

The present study, we investigate the preventive role of naringin, a dietary flavonoid, against ultraviolet-B (UVB) radiation (280-320 nm) induced oxidative damage and inflammatory responses in mouse embryonic fibroblast cell lines (NIH-3T3). In this study, 20 mJ/cm(2) of UVB radiation induces cell cytotoxicity, reactive oxygen species (ROS) generation, DNA damage, and antioxidants depletion in NIH-3T3 cells. Treatment with naringin (60 mu M) prior UVB exposure prevented the cell cytotoxicity, ROS generation, DNA damage, and antioxidants depletion in NIH-3T3 cells. Furthermore, naringin prevents UVB-induced mitogen-activated protein kinase families and nuclear factor-kappa B (NF-kappa B)-mediated activation of inflammatory factors, that is TNF-alpha, IL-6, IL-10, and COX-2 in NIH-3T3 cells. Peroxisome proliferator-activated receptor gamma (PPAR gamma) is an anti-inflammatory agent and it suppressed the UVB-mediated oxidative and inflammatory responses. In this study, naringin activates PPAR gamma and prevents inflammatory biomarkers in NIH-3T3 cells. Thus, naringin prevents UVB-mediated inflammation and oxidative damage in NIH-3T3 cells probably over controlling NF-kappa B expression and activation of PPAR gamma.