Effects Of Mogroside On Oxidative Stress And Related Damage Of Pancreatic Islet β Cell Induced By Palmitic Acid

Objective:Oxidative stress and related damage of pancreatic islet β cell is an important part of pathogenesis mechanism of type2diabetes mellitus. Insulin resistance resulted elevation of serum free fatty acid and triglyceride level. Free fatty acid above normal physiological level induces reactive oxygen species build up and oxidative stress in pancreatic islet P cell through many metabolism pathways. These result in activation of signal transduction pathways related with oxidative stress reactions, reducing glucose metabolism and insulin secretion of pancreatic isletβ cell, even promoting cell death. Using palmitic acid treated NIT-1insulin secreting cell as model of pancreatic islet (3cell oxidative stress related damage under influence of high lipid environment, we study effects and mechanism of action on oxidative stress related damage of mogroside, which has antioxidant and blood glucose control activities proven on animal diabetes model.Methods:Mouse insulinoma cell line NIT-1cells were cultivated in culture media contain palmitic acid, and treated with mogroside. Cell apoptosis ratio and content of reactive oxygen species (ROS) were inspected by flow cytometry, Expressions of Glucose Transporter-2(GLUT2) and pyruvate kinase were examined by semi-quantitate reverse transcript PCR assay.Results:Compare with palmitic acid treated group, mogroside scavenged excessive ROS and lowered its concentration significantly (P<0.05), and expressions of GLUT2and pyruvate kinase are increased (P<0.05), but mogroside is effectless in reducing apoptosis ratio elevated by palmitic acid (P>0.05).Conclusion:Mogroside scavenges excessive ROS induced by palmitic acid, and elevate dampened expressions of GLUT2and pyruvate kinase. This indicated mogroside may accomplish its islet β cell protection effects by reducing ROS within cell and reversing glucose metabolism activity reduction and other effects induced by forkhead box protein-1(FOXO1) activated by oxidative stress. These effects may improve glucose intake and metabolism, and restore normal glucose stimulated insulin secretion (GSIS) function of pancreatic isletβ cell.