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目的 以链脲佐菌素诱导的糖尿病大鼠为实验模型 ,研究内源性一氧化氮合酶 (NOS)抑制物非对称性二甲基精氨酸 (ADMA)升高与糖尿病代谢控制的关系。方法 用高效液相色谱测定大鼠血清ADMA浓度 ;用离体胸主动脉环检测乙酰胆碱诱导的内皮依赖性舒张反应 ;并检测血糖、糖基化血清蛋白和血清脂质过氧化产物丙二醛 (MDA)浓度以反映代谢控制。结果 糖尿病大鼠血清ADMA浓度比正常组大鼠明显升高 ,并伴有离体血管内皮依赖性舒张反应的显著抑制 ;经胰岛素治疗 8wk后 ,不仅阻止内源性ADMA的升高 ,也明显改善血管的内皮依赖性舒张功能。此外 ,糖尿病大鼠血糖、糖基化血清蛋白和血清MDA水平也比正常组明显升高。用胰岛素改善代谢控制后 ,血糖、糖基化血清蛋白和血清MDA水平均恢复正常 ,血中ADMA浓度也显著降低。结论 糖尿病大鼠血中内源性NOS抑制物ADMA浓度升高与代谢控制密切相关 ;胰岛素逆转糖尿病大鼠内源性ADMA升高可能与纠正代谢紊乱和降低脂质过氧化有关
Objective To investigate the relationship between the increase of asymmetric dimethylarginine (ADMA) and the metabolism of diabetes mellitus (DM) induced by streptozotocin in diabetic rats. . Methods Serum ADMA concentration was determined by high performance liquid chromatography. Acetylcholine-induced endothelium-dependent vasodilatation was detected with isolated thoracic aorta rings. Serum glucose, glycosylated serum proteins and serum lipid peroxidation products, malondialdehyde MDA) concentration to reflect metabolic control. Results Serum ADMA levels in diabetic rats were significantly higher than those in normal rats and were significantly inhibited by endothelium-dependent vasodilatation in vitro. Insulin treatment for 8 weeks not only prevented the elevation of endogenous ADMA, but also significantly improved Endothelium-dependent relaxation of blood vessels. In addition, blood glucose, glycosylated serum protein and serum MDA levels in diabetic rats were also significantly higher than the normal group. With insulin to improve the metabolic control, blood glucose, glycosylated serum protein and serum MDA levels returned to normal, the blood ADMA concentration was also significantly reduced. Conclusion The increase of endogenous NOS inhibitor ADMA concentration in blood of diabetic rats is closely related to the metabolic control. The increase of endogenous ADMA induced by insulin in diabetic rats may be related to the correction of metabolic disorders and the decrease of lipid peroxidation