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目的探讨葛根素对高脂诱导的HFD小鼠高血糖水平的影响以及GLP-1R通路在葛根素降糖功效中的作用。方法以高脂诱导的HFD(High-fat-diet)糖尿病小鼠模型为对象,采用GLP-1受体拮抗剂Exendin 9-39(Ex 9-39)用以阻断GLP-1R通路的激活,通过动物体内实验进一步评价GLP-1R通路在葛根素降糖功效中的作用。结果葛根素能够有效降低HFD小鼠血糖水平并改善HFD小鼠口服葡萄糖耐受能力,而Ex 9-39显著抑制葛根素的降糖作用,并且葛根素促进小鼠胰岛素分泌的作用也被Ex 9-39所阻断。通过小鼠胰腺组织切片免疫荧光染色检测观察到,葛根素能够增加HFD小鼠胰岛β细胞中ki67的表达,提示其能够促进胰岛β细胞增殖,当Ex 9-39阻断GLP-1R通路激活时,葛根素的作用被抑制。结论本研究首次在糖尿病小鼠模型中,证实葛根素降糖及改善胰岛β细胞生存的作用依赖于GLP-1R通路的激活,为今后葛根降糖的潜在开发应用奠定实验基础。
Objective To investigate the effect of puerarin on hyperglycemia in HFD induced by high fat and the effect of GLP-1R pathway on the hypoglycemic effect of puerarin. Methods High-fat-induced HFD (high-fat-diet) diabetic mouse model was used to block the activation of GLP-1R pathway by using GLP-1 receptor antagonist Exendin 9-39 (Ex 9-39) The effect of GLP-1R pathway on the hypoglycemic effect of puerarin was further evaluated by in vivo experiments in animals. Results Puerarin can effectively reduce blood glucose levels in HFD mice and improve oral glucose tolerance in HFD mice, whereas Ex 9-39 significantly inhibits the hypoglycemic effect of puerarin and the effect of puerarin on insulin secretion in mice is also influenced by Ex 9 -39 blocked. Immunofluorescence staining of mouse pancreatic tissue sections showed that puerarin increased the expression of ki67 in islet β cells of HFD mice, suggesting that it can promote the proliferation of pancreatic β cells. When Ex 9-39 blocks the activation of GLP-1R pathway , The effect of puerarin is inhibited. Conclusion This study is the first in a mouse model of diabetes mellitus that the hypoglycemic effect of puerarin and the improvement of pancreatic β-cell survival depend on the activation of the GLP-1R pathway, laying an experimental foundation for the potential development and application of pueraria glucose in the future.