Yildiz O, Ozata M, Ozkardeş A, Deniz G, Yildirimkaya M, Corakçi A, Yardim M, Gündoğan M A
Department of Medical Pharmacology, Gülhane School of Medicine, Ankara, Turkey.
Naunyn Schmiedebergs Arch Pharmacol. 1996 Oct;354(4):526-31. doi: 10.1007/BF00168446.
The effects of aminoguanidine (AG) and L-carnitine (LC) on somatosensorial evoked potential (SEP) latency and neural levels of thiobarbituric acid reactive substances (TBARS), products of lipid peroxidation, were compared in alloxan-diabetic rats. AG and LC were given to diabetic rats starting from the 3rd week after the induction of diabetes and lasting for 4 weeks. SEP latency was measured by stimulating via caudal nerve and recording via cortex, once weekly during the treatments. Diabetes caused deficits in SEP (P < 0.05 vs non-diabetic control rats, respectively). AG and LC restored SEP latencies slightly but not significantly, with the exception of the prominent effect of AG at the first week and both treatments at the 4th week of the treatments (P < 0.05 vs untreated diabetic rats, respectively). Diabetes caused elevation in neural TBARS levels (P < 0.05 vs non-diabetic group), which was prevented by both AG and LC (P < 0.05 vs untreated diabetic rats, respectively). Weight and the glucose levels were not influenced by the treatments. Our results suggest that AG improves SEP latencies better than LC. Our results also suggest that the beneficial effects of both AG and LC on diabetic neuropathy are not associated with the regulation of glycemia, but these effects may be related in part with prevention of lipid peroxidation.
在四氧嘧啶诱导的糖尿病大鼠中，比较了氨基胍（AG）和左旋肉碱（LC）对体感诱发电位（SEP）潜伏期以及硫代巴比妥酸反应性物质（TBARS，脂质过氧化产物）神经水平的影响。从糖尿病诱导后的第3周开始，对糖尿病大鼠给予AG和LC，持续4周。在治疗期间，每周通过刺激尾神经并记录皮质电位来测量SEP潜伏期。糖尿病导致SEP出现缺陷（分别与非糖尿病对照大鼠相比，P < 0.05）。AG和LC略微恢复了SEP潜伏期，但不显著，不过在治疗的第1周AG有显著效果，在第4周两种治疗均有显著效果（分别与未治疗的糖尿病大鼠相比，P < 0.05）。糖尿病导致神经TBARS水平升高（与非糖尿病组相比，P < 0.05），AG和LC均可预防这种升高（分别与未治疗的糖尿病大鼠相比，P < 0.05）。治疗对体重和血糖水平没有影响。我们的结果表明，AG比LC能更好地改善SEP潜伏期。我们的结果还表明，AG和LC对糖尿病神经病变的有益作用与血糖调节无关，但这些作用可能部分与预防脂质过氧化有关。
