1. 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.
- Author
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NilamberLal Das R, Muruhan S, Nagarajan RP, and Balupillai A
- Subjects
- Animals, Anti-Inflammatory Agents pharmacology, DNA Damage, Mice, NF-kappa B metabolism, NIH 3T3 Cells, Oxidative Stress radiation effects, Signal Transduction, Flavanones pharmacology, Inflammation drug therapy, Oxidative Stress drug effects, PPAR gamma metabolism, Ultraviolet Rays
- Abstract
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 µM) 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-κB (NF-κB)-mediated activation of inflammatory factors, that is TNF-α, IL-6, IL-10, and COX-2 in NIH-3T3 cells. Peroxisome proliferator-activated receptor γ (PPARγ) is an anti-inflammatory agent and it suppressed the UVB-mediated oxidative and inflammatory responses. In this study, naringin activates PPARγ 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-κB expression and activation of PPARγ., (© 2018 Wiley Periodicals, Inc.)- Published
- 2019
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