摘要
目的研究血管紧张素转换酶抑制剂（ACEI）对糖尿病大鼠周围神经病变的防治作用，并探讨其作用机制。方法链脲佐菌素（STZ）诱导糖尿病大鼠，预防及治疗性给药8周，观察赖诺普利（lisinopril）对坐骨神经传导速度及超微结构的影响；并测定神经组织超氧化物歧化酶（SOD）、丙二醛（MDA）、Na^＋-K^＋-ATPase活性及神经丝蛋白、髓鞘碱性蛋白（MBP）的表达、神经内膜毛细血管密度。结果赖诺普利预防或治疗可不同程度地改善坐骨神经的功能和结构；改善神经组织的氧化应激状态、提高Na^＋-K^＋-ATPase活性、增加神经结构蛋白的表达、促进血管新生。结论ACEI是防治糖尿病周围神经病变的有效措施，其机制可能与改善神经组织缺血及相关代谢紊乱有关。
Objective The aim of this study is to investigate the prevention and therapy effects of ACE inhibitor on diabetic peripheral neuropathy （DPN） in rats and to explore the mechanism. Methods Di- abetes was induced by STZ. After 8 weeks of prevention or treatment, we observed the effects of ACEI （ lisinopril ） on nerve conduction velocity and ultramicrostructure of sciatic nerve ; determined SOD, MDA, Na^＋ -K^＋ - ATPase activity, assessed neurofilament, MBP and capillary density of sciatic nerve. Results Lisinopril prevention/therapy treatment improved nerve structure and function at different degrees; improved oxidative stress state, Na^ ＋ -K^ ＋ -ATPase activity, neurofilameut, MBP expression and angiogenesis. Conclusions ACEI is an effective measurement on DPN. The possible mechanisms were related to its improvement of nerve ischemic state and relative metabolic disorders.
出处
《国际内分泌代谢杂志》
2008年第6期424-428,共5页
International Journal of Endocrinology and Metabolism
