Protective Effects Of Loureirin B On NIT-1Dysfunction Induced By Palmitic Acid

Objective: This study uses palmitic acid to culture pancreatic β-cells(NIT-1cells) in vitro and to simulate the change of the internal environment, whichleads to blood glucose and blood lipid metabolic disorders, caused by oxidativestress. Through use of Loureirin B to intervene the damage to NIT-1cellscasued by palmitic acid, we preliminary discuss the protective effect and itsmechanism of Loureirin B to the NIT-1cells cultured with palmitic acid in virto.Methods: NIT-1cells were the experiment cells. Experimentation weredivided into blank control group, various dose of Loureirin B controlgroup(5μmol/L、10μmol/L and20μmol/L), palmitic acid group, various dose ofLoureirin B intervention group(5μmol/L、10μmol/L and20μmol/L). Cellsviability were inspected by MTT, content of reactive oxygen species (ROS) andcell apoptosis ratio were inspected by flow cytometry, expressions of GlucoseTransporter-2(GLUT2) was examined by semi-quantitate reverse transcriptPCR assay.Results: Comparison with palmitic acid group, activity survival rate ofNIT-1with Loureirin B (10μmol/L and20μmol/L) intervention group, risestrikingly（p＜0.05). ROS and the cell apoptosis ratio of NIT-1with LoureirinB(5μmol/L、10μmol/L and20μmol/L) intervention group were decrease strikingly（p＜0.05).20μmol/L of Loureirin B could increase the expressions ofGLUT-2（p＜0.05），the expressions of GLUT-2with5μmol/L and10μmol/L ofLoureirin B had no clear change（p＞0.05).Conclusions: Palmitic acid could restrain the cell proliferation of NIT-1,made intracellular active oxygen free radicals (ROS) increased，and lead to cellsto produce oxidative stress, cell apoptosis rate increased, the relative reductionof expression of sugar metabolism related gene (GLUT-2) in intracellular,consequently, affect cell sugar metabolism. Loureirin B could increase theactivity survival rate of NIT-1in the cultivate with palmitic acid，NIT-1intracellular ROS levels were decrease strikingly, decrease the cell apoptosisresult in free fatty acids. Loureirin B of20μmol/L could striking up-regulationencoding gene of dampened GLUT-2, its mechanism maybe reduceintra-cellular ROS, decrease the cell apoptosis result in free fatty acids, andbring into play protecte NIT-1.