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目的:观察α-亚麻酸(ALA)对糖尿病(DM)大鼠血管功能和氧化应激的影响,探讨ALA在DM血管并发症防治中的作用。方法:将30只SD大鼠随机分为正常对照组、DM模型组和ALA治疗组[500μg/(kg.d)],每组10只。10只雄性SD大鼠以高脂饮食喂养4周后,腹腔注射链脲佐菌素(STZ)30 mg/kg建立Ⅱ型DM(T2DM)模型。4周后分离降主动脉,进行离体血管灌流观察血管的舒张功能,利用试剂盒测定灌流液中NO的含量以及血管组织中丙二醛(MDA)的含量、超氧化物岐化酶(SOD)和过氧化氢酶(CAT)的活性。结果:与正常对照组相比,DM大鼠主动脉内皮依赖性舒张功能和NO的含量显著下降(P<0.01),ALA治疗可有效地减轻DM大鼠血管内皮功能障碍,增加NO的含量(均P<0.01)。另外,与正常对照组相比,DM大鼠血管组织中MDA的含量增加(P<0.01),抗氧化酶SOD和CAT的活性下降(P<0.01);ALA治疗可显著降低DM大鼠血管组织中MDA的含量(P<0.05),增加抗氧化酶SOD和CAT的活性(P<0.01)。结论:ALA可显著改善T2DM模型大鼠的血管内皮舒张功能障碍,其机制可能与减轻血管组织的氧化应激有关。
Objective: To observe the effects of α-linolenic acid (ALA) on vascular function and oxidative stress in diabetic rats and to explore the role of ALA in the prevention and treatment of diabetic vascular complications. Methods: Thirty SD rats were randomly divided into normal control group, DM model group and ALA treatment group [500μg / (kg · d)], with 10 rats in each group. Ten male SD rats fed a high-fat diet for 4 weeks were injected intraperitoneally with streptozotocin (STZ) 30 mg / kg to establish type II DM (T2DM) model. After 4 weeks, the descending aorta was isolated and the vasodilatory function was observed by perfusion in vitro. The content of NO in perfusate and the content of malondialdehyde (MDA) in vascular tissue were detected by kit, the activities of superoxide dismutase (SOD) ) And catalase (CAT) activity. Results: Compared with normal control group, endothelium-dependent vasodilatation and NO content in DM rats decreased significantly (P <0.01). ALA treatment could effectively reduce vascular endothelial dysfunction and increase NO level in DM rats All P <0.01). In addition, compared with the normal control group, the content of MDA in vascular tissue of diabetic rats increased (P <0.01) and the activity of antioxidant enzymes CAT and CAT decreased (P <0.01). ALA treatment significantly reduced the levels of MDA (P <0.05), and increased the activity of antioxidant enzymes SOD and CAT (P <0.01). Conclusion: ALA can significantly improve the vascular endothelial dysfunction in T2DM rats, which may be related to the reduction of oxidative stress in vascular tissues.