α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage

Abstract

Abstract. Previous studies have demonstrated an association between neurological diseases and oxidative stress (OS).Naphthoflavone is a synthetic derivative of naturally occurring flavonoids that serves an important role in the treatment and prevention of OS-related diseases. The current study was designed to apply α-and β-Naphthoflavone individually and in combination to counteract the detrimental effects of OS on neurons in vitro. Neuronal SH-SY5Y cells were subjected to 20 µM H 2 O 2 , followed by exposure to 20 µM α-Naphthoflavone and/or 10 µM β-Naphthoflavone. Results indicated that α-and β-Naphthoflavone effectively antagonized the apoptosis-promoting effect of H 2 O 2 on neuronal SH-SY5Y cells, and that β-Naphthoflavone significantly (P<0.05) reversed H 2 O 2 -inhibited cell viability. Notably, co-treatment of α-and β-Naphthoflavone reversed the H 2 O 2 -induced apoptosis rate elevation and cell viability reduction. Further analysis demonstrated that H 2 O 2 inhibited the activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase, but this was reversed by the co-treatment with α-and β-Naphthoflavone and selectively enhanced by the treatment with α-or β-Naphthoflavone. H 2 O 2 -stimulated p38 mitogen-activated protein kinase activation was repressed following treatment with α-and/or β-Naphthoflavone, along with a decreased expression of the apoptosis-related factors and inhibited caspase-3 activation. In conclusion, co-treatment with α-and β-Naphthoflavone minimized H 2 O 2 -led neuron damage compared with treatment with α-or β-Naphthoflavone, suggesting a synergetic effect between α-and β-Naphthoflavone. This indicates that utilizing α-and β-Naphthoflavone together in the clinical setting may provide a novel therapeutic for neurological disease.

β-Naphthoflavone Activation of the Ah Receptor Alleviates Irradiation-Induced Intestinal Injury in Mice

“…Previous studies demonstrate that BNF upregulates the expression or activity of antioxidative enzymes, including glutathione peroxidase, quinone oxidoreductase-1, glutathione transferase and heme oxygenase-1 [ 9 ], and represses ROS-producing enzymes such as NADPH oxidase [ 10 ]. This suggests BNF potentially affects antioxidation [ 11 ]. In the present work, we show that BNF as an AhR agonist protects against oxidative DNA damage in the rat intestinal epithelial cell (IEC-6), while the ROS scavenging system is not involved.…”