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、50 μmol/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、50 μmol/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、50 μmol/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50 μmol/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/c-Met通路有关。

Objective To investigate the effects of cyanidin-3-O-glucoside on the damage of pancreatic islet β cells induced by high glucose and high fat and its mechanism. Methods Islet β cells were treated with different concentrations (10, 20, 30, 40, and 50 μmol/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 50 μmol/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 pancreatic β cells (P＜0.05). Compared with model group, the cell viability of cyanidin-3-O-glucoside 10 and 50 μmol/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 50 μmol/L group was better than that of cyanidin-3-O-glucoside 10 μmol/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 pancreatic β cells induced by high glucose and high fat, increase insulin secretion and inhibit oxidative stress damage, which is related to the activation of HGF/c-Met pathway.

R965

新疆维吾尔族自治区自然科学基金项目（2022D01C221）