目的 研究葛根素对体内外晚期糖基化终末产物（AGEs）形成的影响。方法 C57BL/6小鼠采用高糖高脂饲料联合链脲佐菌素（40 mg/kg）构建糖尿病模型。造模成功后随机分为模型组，氨基胍组（100 mg/kg），葛根素低、中、高剂量（50、100、200 mg/kg）组，另设对照组。连续给药8周后，检测空腹血糖（FBG）、口服糖耐量（OGTT）、糖化血清蛋白（GSP）及血清AGEs水平。此外将不同浓度的葛根素（0.5、1.0、2.0 mmol/L）与丙酮醛和牛血清白蛋白共孵育144 h，建立体外非酶糖基化反应模型，用荧光光度法测定AGEs的荧光值，考察葛根素体外抑制AGEs生成的规律。结果 葛根素能够显著降低糖尿病小鼠的FBG，改善OGTT，抑制GSP及血清AGEs的生成。葛根素在体外非酶糖基化反应体系中抑制AGEs的生成，并有一定的剂量依赖性。结论 葛根素可以显著降低糖尿病小鼠的FBG，对体内外AGEs的形成具有明显的抑制作用。

Objective To study the influence of puerarin on advanced glycation end products (AGEs) formation in vivo and in vitro. Methods C57BL/6 mice were fed with high fat diet and injected with streptozotocin (40 mg/kg) to establish diabetic model. After modeling, mice were randomly divided into blank control group, model group, aminoguanidine group (100 mg/kg), low-, mid-, and high-dose puerarin (50, 100, and 200 mg/kg) groups. After treatment of eight weeks, the levels of fasting blood-glucose (FBG), oral glucose tolerance test (OGTT), glycated serum protein (GSP), and AGEs in serum were detected. To establish non-enzymatic glycation reaction model in vitro, glucose and bovine serum albumin (BSA) were incubated with puerarin at different concent rations respectively for 144 h. The productivity of non-enzymatic advanced glycation end products was detected by aspectrophotometer. Results Puerarin can significantly lower the level of FBG and oral glucose tolerance in diabetic mice, and inhibit the productivity of GSP and AGEs in serum. Besides, puerarin also significantly inhibits the productivity of AGEs in vitro in a concentration-dependent manner. Conclusion Puerarin possesses significant inhibitory effect on the productivity of AGEs in vivo and in vitro.

国家自然科学基金资助项目（81473394）；镇江市2015年第四批科技计划（重点研发计划——社会发展）项目（SH2015068）；江苏省青年医学人才项目（QNRC2016634）；江苏省“333高层次人才培养工程”项目；江苏省“六大高峰人才”项目（YY-012）