目的 研究头花蓼的降糖作用靶点。方法 采用人源肝癌HepG2细胞，检测细胞经头花蓼提取物（PCB）作用后培养液上清中葡萄糖的量。采用qRT-PCR检测PCB对HepG2细胞过氧化物酶体增殖物激活受体-α（PPAR-α）、葡萄糖转运蛋白4（GLUT4）基因表达的影响。采用与胰岛β细胞功能相似的大鼠胰岛细胞瘤INS-1细胞，分为药物保护组和修复组，检测PCB对链脲佐菌素（STZ）损伤的INS-1细胞的保护和修复作用。MTT法检测INS-1细胞的增殖活力、生化法检测细胞内超氧化物歧化酶（SOD）和丙二醛（MDA）水平，Western blotting法检测INS-1细胞Cyt C、Caspase-3蛋白表达水平。采用麦芽糖为底物的α-葡萄糖苷酶抑制模型，测定PCB对α-葡萄糖苷酶的抑制率。结果 PCB显著促进HepG2细胞对上清中葡萄糖的吸收，且显著上调PPAR-α、GLUT4基因表达（P<0.001）。对STZ损伤的INS-1细胞的保护和修复实验中，相比于模型组，PCB组细胞活力显著增加（P<0.01、0.001），升高SOD水平，降低MDA水平（P<0.05），同时显著降低Cyt C、Caspase-3蛋白表达水平（P<0.001）。PCB对α-葡萄糖苷酶有抑制活性，IC₅₀为11.53 mg/mL。结论 PCB可通过上调PPAR-α、GLUT4基因表达促进HepG2细胞对上清中葡萄糖的吸收；通过阻碍Cyt C-Caspase-3通路减少STZ损伤的INS-1细胞凋亡；通过升高SOD、降低MDA改善INS-1细胞氧化应激；对α-葡萄糖苷酶有抑制活性。

Objective To investigate the hypoglycemic targets of Polygonum capitatum. Methods Human liver cancer HepG2 cells were adopted to detect the supernatant culture medium glucose content, and the effect on PPAR-α and GLUT4 gene expression was investigated by qRT-PCR after treatment of P. capitatum extracts (PCB). INS-1 cells similar to islet β cells, divided into drug protection group and repair group, were adopted to determine the cell proliferation activity by MTT; The intracellular SOD and MDA levels were measured by biochemical method; The Cyt C and Caspase-3 protein expression levels were detected by Western blotting. Adopting maltose as substrate of α-glycosidase enzyme inhibition model, the inhibitory efficiency of PCB on glycosidic enzyme was determined. Results PCB group significantly promoted the absorption of HepG2 cells to supernatant glucose and increased the expression of PPAR-α and GLUT4 genes significantly. Aim at protection and repair of INS-1 cells, PCB group significantly increased cell vitality and SOD level, reduced MDA level compared with model group, and at the same time significantly reduced Cyt C and Caspase-3 protein expression levels. PCB had inhibitory activity to α-glycosidase enzymes, with IC₅₀ of 11.53 mg/mL. Conclusion PCB could significantly increase the PPAR-α and GLUT4 genes expression to promote the absorption of HepG2 cells to supernatant glucose by blocking the Cyt C-Caspase-3 pathways to reduce apoptosis of islet cells which were damaged by STZ and by raising SOD and declining MDA to improve INS-1 cell oxidative stress; What's more it has inhibitory activity to α-glycosidase enzymes.

浙江省自然科学基金资助项目（LY16H280010）