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目的:探讨胰岛素抵抗大鼠模型血压升高的机制。方法:通过给予高糖饮食及NG-硝基-左旋-精氨酸-甲基酯(L-NAME)喂养建立不同的胰岛素抵抗大鼠模型,观察大鼠血压及血清内皮型一氧化氮合成酶(eNOS)、一氧化氮(NO)、超氧化物歧化酶(SOD)、超氧阴离子(O2-)和血浆血管紧张素Ⅱ(AngⅡ)的变化。结果:实验前各组大鼠血压差异无统计学意义(P>0.05),而实验4周时,高糖组、L-NAME组的血压均明显高于对照组(均P<0.01)。高糖组(P<0.05)和L-NAME组(P<0.01)NO水平均低于对照组,而O2-升高(均P<0.05)。L-NAME组的eNOS活性低于对照组(P<0.05),高糖组与对照组相比,差异无统计学意义(P>0.05)。与对照组相比,高糖组大鼠血清SOD活性明显降低(P<0.01)。各组大鼠AngⅡ水平与对照组相比差异无统计学意义(P>0.05)。结论:NO水平下降和氧化应激引起NO生物活性降低,在胰岛素抵抗大鼠模型高血压的发病机制中发挥重要作用。
Objective: To investigate the mechanism of hypertension in insulin resistance rat model. METHODS: Different models of insulin resistance were established by feeding high glucose diet and feeding NG-nitro-L-arginine-methyl ester (L-NAME). Blood pressure and serum level of endothelial nitric oxide synthase (eNOS), nitric oxide (NO), superoxide dismutase (SOD), superoxide anion (O2-) and plasma angiotensin Ⅱ (Ang Ⅱ). Results: Before the experiment, there was no significant difference in blood pressure between the two groups (P> 0.05). At 4 weeks, the blood pressure of high glucose group and L-NAME group were significantly higher than that of the control group (all P <0.01). The levels of NO in high glucose group (P <0.05) and L-NAME group (P <0.01) were lower than those in control group, while O2- increased (all P <0.05). The activity of eNOS in L-NAME group was lower than that in control group (P <0.05). There was no significant difference between high glucose group and control group (P> 0.05). Compared with the control group, the activity of SOD in serum of high glucose group was significantly decreased (P <0.01). There was no significant difference in AngⅡ level between the two groups (P> 0.05). CONCLUSION: The decrease of NO level and the decrease of NO bioactivity caused by oxidative stress play an important role in the pathogenesis of hypertension in insulin resistance model rats.