摘要
目的 探究矢车菊素-3-O-葡萄糖苷对高糖高脂诱导的胰岛β细胞损伤的影响及机制。方法 使用不同浓度(10、20、30、40、50μmol/L)矢车菊素-3-O-葡萄糖苷处理胰岛β细胞,CCK-8法检测细胞活力;将胰岛β细胞分为对照组、模型组及矢车菊素-3-O-葡萄糖苷10、50μmol/L组,CCK-8法检测各组细胞活力,酶联免疫吸附法(ELISA)测定各组细胞胰岛素分泌量,DCFH-DA荧光探针法检测各处理组细胞活性氧(ROS)水平,比色法检测各处理组细胞超氧化物歧化酶(SOD)活性与丙二醛(MDA)含量,蛋白质免疫印迹(Western blotting)法检测各处理组细胞肝细胞生长因子(HGF)/间质表皮转化因子受体(c-Met)通路相关蛋白表达水平。使用c-Met抑制剂SU11274进行干预,实验将胰岛β细胞分为对照组、模型组、矢车菊素-3-O-葡萄糖苷组、矢车菊素-3-O-葡萄糖苷+SU11274组,再通过CCK-8法检测各处理组细胞活力,ELISA法测定各组细胞胰岛素分泌量。结果 与对照组比较,不同浓度矢车菊素-3-O-葡萄糖苷作用均显著提高了胰岛β细胞活力(P<0.05)。与模型组比较,矢车菊素-3-O-葡萄糖苷10、50μmol/L组的细胞活力显著升高,胰岛素分泌水平显著增加,细胞内ROS水平和MDA含量显著降低,SOD活性显著升高,HGF、p-c-Met/c-Met蛋白水平显著上调(P<0.05),且矢车菊素-3-O-葡萄糖苷50μmol/L组改善更显著(P<0.05)。使用c-Met抑制剂SU11274干预后,与矢车菊素-3-O-葡萄糖苷组比较,矢车菊素-3-O-葡萄糖苷+SU11274组细胞活力则显著降低,胰岛素分泌水平显著减少(P<0.05)。结论 矢车菊素-3-O-葡萄糖苷能够提高高糖高脂诱导下胰岛β细胞的活力,增加其胰岛素分泌量,并抑制氧化应激损伤,该作用与激活HGF/cMet通路有关。
Objective To investigate the effects of cyanidin-3-O-glucoside on the damage of pancreatic isletβcells induced by high glucose and high fat and its mechanism.Methods Isletβcells were treated with different concentrations(10,20,30,40,and 50μmol/L)of cyanidin-3-O-glucoside,and cell viability was detected by CCK-8 method.The experiment was divided into control group,model group,cyanidin-3-O-glucoside 10 and 50μmol/L group,the cell viability of each group was detected by CCK-8 method,the insulin secretion of each group was determined by ELISA method,the level of ROS was detected by DCFH-DA fluorescent probe,the SOD and MDA were detected by colorimetry,the expression levels of HGF/c-Met pathway related proteins were detected by Western blotting.In the pathway study,c-Met inhibitor SU11274 was used to intervene,and the experiment was divided into control group,model group,cyanidin-3-O-glucoside group,and cyanidin-3-O-glucoside+SU11274 group,the cell vitality of each group was detected by CCK-8 method,and the insulin secretion of cells in each group was determined by ELISA method.Results Compared with control group,different concentrations of cyanidin-3-O-glucoside significantly increased the activity of pancreaticβcells(P<0.05).Compared with model group,the cell viability of cyanidin-3-O-glucoside 10 and 50μmol/L group were significantly increased,and the level of insulin secretion was significantly increased,ROS level and MDA content were significantly decreased,SOD activity was significantly increased,HGF and p-c-Met/c-Met protein levels were significantly up-regulated(P<0.05),and the effect of cyanidin-3-O-glucoside 50μmol/L group was better than that of cyanidin-3-O-glucoside 10μmol/L group(P<0.05).After the intervention with c-Met inhibitor SU11274,compared with cyanidin-3-O-glucoside group,the cell viability and insulin secretion levels in cyanidin-3-O-glucoside+SU11274 group were significantly decreased(P<0.05).Conclusion Cyanidin-3-O-glucoside can enhance the activity of pancreaticβcells induced by hig
作者
马存花
高静
MA Cunhua;GAO Jing(Department of Endocrinology,the Fifth Affiliated Hospital of Xinjiang Medical University,Urumqi 830000,China)
出处
《现代药物与临床》
CAS
2024年第1期1-7,共7页
Drugs & Clinic
基金
新疆维吾尔自治区自然科学基金项目(2022D01C221)。
