氨基胍改善糖尿病神经病变及作用机制分析

目的　观察氨基胍对遗传突变型糖尿病小鼠 (db/d小鼠)坐骨神经传导速度减慢是否有改善作用,并分析其作用机制。方法　采用澳洲AD公司powerlab/8s多用生理记录仪测定db/db小鼠坐骨神经传导速度。结果　6mon龄db/db小鼠用氨基胍治疗五个月后相对于同年龄模型对照组坐骨神经传导速度明显加快 (P<0 05 )。同时体内晚期糖基化终产物(AGEs)的含量也明显降低。结论　氨基胍可能通过降低体内AGEs的含量来防止db/db小鼠坐骨神经传导速度的减慢。

Study on amelioration of aminoguanidine on diabetic neuropathy and its mechanism

Aim To determine whether aminoguanidine increases the motor nev e conduction velocity of db/db mice and why. Mothods Motor neve conduc tion velocity was assayed by Powerlab/8s multipurpose physiological recorder. Ad vanced glycosylation end products of db/db mice kidney were determined by fluoro meter. Results Motor neve conduction velocity of 6 months db/db mic e treated with Aminoguanidine for 5 months increased significantly. Conclu sion Aminoguanidine can prevent the decrease of the motor neve conduction v elocity of db/db mouse by decreasing the advanced glycosylation end products.