罗汉果甜苷干预棕榈酸致胰岛B细胞氧化应激相关损伤的机制研究

Mechanism of Morgroside Intervening in Related Oxidative Stress Damage of Pancreatic Islet B Cell Induced by Palmitic Acid

目的:研究罗汉果甜苷干预棕榈酸致胰岛B细胞氧化应激相关损伤的机制。方法:以小鼠胰岛B细胞系NIT-1细胞作为细胞模型。实验分为空白对照、罗汉果甜苷对照、模型、罗汉果甜苷干预4组,使用流式细胞术测定细胞内活性氧自由基(ROS)含量和细胞凋亡率,半定量逆转录PCR测定葡萄糖转运受体(GLUT)-2和丙酮酸激酶编码基因表达水平。结果:与模型组比较,罗汉果甜苷组NIT-1细胞内ROS含量显著降低,GLUT-2和丙酮酸激酶编码基因的表达水平显著增强(P<0.05),细胞凋亡无显著改变(P>0.05)。结论:罗汉果甜苷可显著降低NIT-1细胞内ROS水平,显著上调受抑制的GLUT-2和丙酮酸激酶编码基因表达,其机制可能是通过降低细胞内ROS含量,逆转由氧化应激激活的转录因子叉头框蛋白-1(FOXO1)导致的葡萄糖代谢障碍和其他效应,产生对胰岛B细胞的保护作用。

OBJECTIVE： To study the mechanism of morgroside intervening in related oxidative stress damage of pancreatic islet B cell induced by palmitic acid. METHODS： NIT-1 cell lines of mice were used model. Mice were divided into 4 groups, i.e. blank control group, morgroside control group, model group and morgroside group. Cell apoptosis ratio and content of reactive oxygen species （ROS） were inspected by flow cytometry, and the expressions of GLUT2 and pyruvate kinase were examined by semi-quantitative reverse transcript PCR essay. RESULTS： Compare with model group, ROS content of NIT-1 cells in morgroside group decreased significantly, and expressions of GLUT2 and pyruvate kinase increased significantly （P〈0.05）, but no significant change was found in cell apoptosis （P〉0.05）. CONCLUSION： Mogroside can decrease the content of ROS in NIT-1 cells, and elevate gene expressions of GLUT2 and pyruvate kinase. This indicated morgroside may protect islet B cell by reducing ROS content and reversal glucose metabolism activity reduction and other effects induced by forkhead box protein-1 （FOXO1） activated by oxidative stress.