黄芪多糖对人心脏微血管内皮细胞缺氧再复氧损伤后核因子-κB表达的影响

目的:观察人心脏微血管内皮细胞(HCMEC)缺血再灌注损伤后核因子-κB(NF-κB)的表达变化,探讨黄芪多糖治疗心肌缺血再灌注损伤的机制。方法:以体外缺氧再复氧复制缺血再灌注损伤模型。免疫细胞化学染色法观察NF-κB的蛋白分布,荧光实时定量PCR检测NF-κB mRNA的表达。结果:缺氧再复氧后,NF-κB发生核转位,其mRNA表达较正常对照组明显增加(P<0.05)。黄芪多糖可抑制NF-κB的核转位,并降低NF-κBmRNA的表达,其中黄芪多糖50μg/mL剂量组降低NF-κBmRNA表达的作用与缺氧再复氧组比较差异显著(P<0.05)。结论:黄芪多糖通过抑制缺氧再复氧后HCMEC的NF-κB信号通路,降低炎症相关基因的激活,从而减轻心肌缺血再灌注损伤时的炎症反应。

Effect of Astragalus Polysaccharide on Expression of Nuclear Factor - κB in Human Cardiac Microvascular Endothelial Cells after Hypoxia and Reoxygenation Injury

Objectives: To observe the expression of nuclear factor-κB(NF-κB) in human cardiac microvascular endothelial cells that were damaged after Hypoxia and Reoxygenation and to explore the mechanism of astragalus polysaccharide(APS) on reducing myocardial ischemia and reperfusion injury.Methods:The ischemia and reperfusion injury model was established by oxygen deprivation and recovery method.Using immunocytochemical stain method to observe the location of NF-κB protein and applying fluorescence quantitative polymerase chain reaction method to detect the expression of NF-κB mRNA.Results: The NF-κB metastasized to cell nuclear after hypoxia/reoxygenated and expression of its mRNA increased obviously compared with the control group(P<0.05).APS could inhibit nuclear metastasis of NF-κB and reduce the expression of NF-κB mRNA,and there was significant difference between 50μg/mL of APS group compared with hypoxia/reoxygenated group(P<0.05).Conclusion:APS could influence the activation of inflammatory related gene through inhibiting the NF-κB signal transduction pathway,thus alleviating the inflammation reaction of myocardial reperfusion injury.