葛根素对D-半乳糖诱导糖基化大鼠脑损害的干预作用

目的：研究葛根素(puerarin, Pue)对D-半乳糖诱导的糖基化模型大鼠并发脑损害的干预作用。方法：D-半乳糖（150 mg·kg^-1·d^-1,ip）给药8周,诱导糖基化模型大鼠,并于第3周开始给予葛根素高、中、低（300,150,75 mg·kg^-1）剂量处理6周。测定红细胞醛糖还原酶活性、糖化血红蛋白、血清果糖胺和晚期糖基化终末产物(AGEs)含量及脑组织中AGEs含量、脑神经细胞内钙离子水平,并以透射电镜观察脑内海马神经细胞线粒体的变化。结果：葛根素高、中剂量明显降低模型组大鼠红细胞醛糖还细胞酶活性,抑制糖化产物的形成（P<0.01）,降低脑组织中AGEs及脑细胞内钙的含量（P<0.05,P<0.01）,保护海马神经细胞线粒体结构的完整性。结论：葛根素具有抑制D-半乳糖诱导的蛋白糖基化反应,并对糖基化状态并发的脑神经细胞损害具有保护作用。

Improvement effects of puerarin on glycated brain damages in rats induced by D-galactose

OBJECTIVE: To observe the improvement effects of puerarin on glycated brain damages in rat model induced by D-galactose. METHOD: The model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks, and all rats were treated with puerarin (high dose 300 mg x kg(-1), middle dose 150 mg x kg(-1), low dose 75 mg x kg(-1)) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products (fructosamine in serum, glycohaemoglobin, advanced glycation end-products) and AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope. RESULT: High dose and middle dose of puerarin can decrease the activity of aldose reductase in red blood cells (P < 0.01), and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P < 0.01). Also, puerarin can decrease the content of AGEs in brain and the level of calcium ions in brain cells (P < 0.05, P < 0.01), and decrease lesions degree in mitochondria in brain hippocampus cells. CONCLUSION: Puerarin can produce the protective effects on glycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.