Hispidin Isolated from Phellinus linteus Protects Against Hydrogen Peroxide-Induced Oxidative Stress in Pancreatic MIN6N β-Cells

Reactive oxygen species (ROS) have been shown to cause DNA damage, protein denaturation, loss of anti-oxidative enzyme activity, and lipid peroxidation. Thus, ROS are associated with tissue damage and are considered to be prime contributing factors in inflammation, diabetes, aging, and cancer. In this study, we investigated whether or not hispidin protects pancreatic MIN6N beta-cells from oxidative stress caused by hydrogen peroxide. Treatment of MIN6N beta-cells with 0.5 mM hydrogen peroxide for 4 hours caused significant loss of cell viability and an increase in the number of apoptotic cells. However, pretreatment of MIN6N beta-cells with hispidin for 24 hours reduced loss of cell viability and decreased the number of apoptotic cells. In addition, 70 mu M hispidin significantly scavenged intracellular ROS and inhibited apoptosis and caspase-3 induced by hydrogen peroxide. Furthermore, the generation of thiobarbituric acid-reactive substances was inhibited in the presence of hispidin in a dose-dependent manner. Also, 70 mu M hispidin significantly increased insulin secretion in hydrogen peroxide-treated MIN6N beta-cells. These results suggest that hispidin may be effective for protecting MIN6N beta-cells from ROS toxicity in diabetes.