Abstract
Reactive oxygen species (ROS) has been implicated as a contributor to both the onset and the progression of diabetes, however how does redox state affect diabetes has not been fully understood. Here we study the role of redox interference on pancreatic mitochondria and the progression of diabetes. We applied streptozotocin (STZ) to establish diabetes mellitus (DM) model in rats, applied FeSO4 to produce oxidative stress (OS) and Ganoderma lucidum polysaccharides as antioxidant intervention (AO). Our results showed that in OS and DM group, oxidative stress caused the imbalance of redox state, resulting in higher lipid peroxidation level and lower antioxidant level, while AO treatment group reduced blood glucose by repairing the redox balance. The insulin level has the order of Normal Control (NC)<AO < DM < OS, suggesting oxidative stress promoted insulin secretion in a compensatory mechanism. The Mn-SOD expression in OS groups of pancreas were significantly lower than other groups, while the p53 expression was significantly higher. The mitochondrial ultrastructure of pancreatic β cells were impaired in DM group, and the damage was more severe in OS group, paralleled with significantly reduced secretory granules, both of which were repaired in the AO group. Our results demonstrated that the redox state can affect the blood glucose of diabetic rats, and oxidative stress can aggravate diabetes, while the early antioxidant treatment can alleviate the process of diabetes through reversing the imbalance of redox state and repairing the pancreatic mitochondria. These results suggest that redox balance plays an important role in the treatment of diabetes.