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急性血糖波动对心肌细胞核因子κB及其抑制因子IκB表达的影响 被引量:6

Acute blood glucose fluctuation has effect on the expression of nuclear factor kappa B and inhibitor of nuclear factor kappa B in myocardial cells
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摘要 目的:探讨急性血糖波动对心肌细胞核因子κB(NF-κB)及其抑制因子IκB表达的影响和临床意义。方法:给Wistar雄性大鼠间断输注50%葡萄糖注射液48h的方法,建立急性血糖波动动物模型。采用比色法检查血清丙二醛、超氧化物歧化酶;免疫组化的方法检测心肌细胞浆中IκB、核中NF-κB表达。结果:急性血糖波动组心肌细胞中NF-κB、IκB、NF-κB/IκB的表达显著升高;急性血糖波动组血清丙二醛、超氧化物歧化酶明显升高。血糖波动组MDA/SOD比值显著高于对照组及持续性高血糖组。结论:急性血糖波动与持续性高血糖都能导致机体的氧化应激水平显著升高,急性血糖波动导致的氧化应激反应更强;增强的氧化应激促进细胞核NF-κB表达,导致心肌炎症反应的发生。 Objective:To investigate that acute blood glucose has the effect on the expression of nuclear factor kappa B(NF-κB)and the inhibitor of NF-κB(IκB).Method:The wistar rats were infused intermittently or consistently with 50% glucose solution.The level of maleic dialdehyde(MDA)and superoxide dismutase(SOD)was investigated through colorimetry.The expression of NF-κB and IκB in myocardial cells was investigated through the method of immunohistochemisty.Result:The expression of NF-κB in the nuclei and IκB in the cytoplasm in myocardial cells in fluctuative blood glucose group was evidently lower than that of consistently high blood glucose group,and the ratio of NF-κB to IκB of fluctuative blood glucose group and consistently high blood glucose group was evidently higher than control group,but there's no stastistical difference between the two groups.The level of serum MDA and SOD of fluctuative blood glucose group was evidently higher than consistently high blood glucose group,and the ratio of MDA to SOD was also evidently higher than that consistently of high blood glucose group.Conclusion:The level of oxidative stress induced by fluctuative blood glucose and consistently high blood glucose group was apparently higher,which activated the expression of NF-κB in the nuclei.
出处 《陕西医学杂志》 CAS 2010年第3期268-270,共3页 Shaanxi Medical Journal
基金 辽宁省教育委员会基金支持项目(20060999)
关键词 心肌疾病/免疫学 血糖/分析 NF-κB/分析 @核因子抑制因子IκB 大鼠 Myocadial diseases/immunology Blood glucose/analysis NF-κappa B/analysis @Inhibitor of NF-κappa B Rats
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二级参考文献7

共引文献3

同被引文献39

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