目的 探究矢車菊素-3-O-葡萄糖苷對高糖高脂誘導的胰島β細胞損傷的影響及機制。方法 使用不同濃度（10、20、30、40、50 μmol/L）矢車菊素-3-O-葡萄糖苷處理胰島β細胞，CCK-8法檢測細胞活力；將胰島β細胞分為對照組、模型組及矢車菊素-3-O-葡萄糖苷10、50 μmol/L組，CCK-8法檢測各組細胞活力，酶聯(lián)免疫吸附法（ELISA）測定各組細胞胰島素分泌量，DCFH-DA熒光探針法檢測各處理組細胞活性氧（ROS）水平，比色法檢測各處理組細胞超氧化物歧化酶（SOD）活性與丙二醛（MDA）含量，蛋白質免疫印跡（Western blotting）法檢測各處理組細胞肝細胞生長因子（HGF）/間質表皮轉化因子受體（c-Met）通路相關蛋白表達水平。使用c-Met抑制劑SU11274進行干預，實驗將胰島β細胞分為對照組、模型組、矢車菊素-3-O-葡萄糖苷組、矢車菊素-3-O-葡萄糖苷＋SU11274組，再通過CCK-8法檢測各處理組細胞活力，ELISA法測定各組細胞胰島素分泌量。結果 與對照組比較，不同濃度矢車菊素-3-O-葡萄糖苷作用均顯著提高了胰島β細胞活力（P＜0.05）。與模型組比較，矢車菊素-3-O-葡萄糖苷10、50 μmol/L組的細胞活力顯著升高，胰島素分泌水平顯著增加，細胞內ROS水平和MDA含量顯著降低，SOD活性顯著升高，HGF、p-c-Met/c-Met蛋白水平顯著上調（P＜0.05），且矢車菊素-3-O-葡萄糖苷50 μmol/L組改善更顯著（P＜0.05）。使用c-Met抑制劑SU11274干預后，與矢車菊素-3-O-葡萄糖苷組比較，矢車菊素-3-O-葡萄糖苷＋SU11274組細胞活力則顯著降低，胰島素分泌水平顯著減少（P＜0.05）。結論 矢車菊素-3-O-葡萄糖苷能夠提高高糖高脂誘導下胰島β細胞的活力，增加其胰島素分泌量，并抑制氧化應激損傷，該作用與激活HGF/c-Met通路有關。

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

新疆維吾爾族自治區(qū)自然科學基金項目（2022D01C221）