摘要
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。
Objectives ： To observe the expression of nuclear factor -kB（ NF -kB） 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 - kB protein and applying fluorescence quantitative polymerase chain reaction method to detect the expression of NF - kB mRNA. Results ： The NF - kB 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 -kB and reduce the expression of NF -kB 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 - kB signal transduction pathway, thus alleviating the inflammation reaction of myocardial reperfusion injury.
出处
《辽宁中医杂志》
CAS
北大核心
2008年第1期7-9,共3页
Liaoning Journal of Traditional Chinese Medicine
基金
国家自然科学基金资助项目(30572391)
关键词
黄芪多糖
微血管内皮细胞
缺氧
复氧
核因子-κB
astragalus polysaccharide
microvascular endothelial cells
hypoxia
reoxygenation
nuclear factor - kB
