CAJ | 학술논문

目的观察葡萄糖对内皮祖细胞(EPC)表达低氧诱导因子1α(HIF-1α)和血管内皮生长因子(VEGF)的影响.方法在EPC培养体系中加入不同浓度葡萄糖,分别在常氧(21%氧浓度)和低氧(1%氧浓度)条件下培养.检测各组HIF-1α及VEGF的基因和蛋白表达水平.结果葡萄糖浓度相同,低氧组表达HIF-1α mRNA高于常氧组,VEGF的表达无统计学差异;氧浓度相同,10mmol/L葡萄糖组EPC表达HIF-1α mRNA高于其余两组,且随着葡萄糖浓度增加,VEGF表达逐渐下降.常氧浓度下测不到HIF-1α蛋白表达;低氧浓度下,10mmol/L葡萄糖组EPC表达HIF-1α最高.结论高糖对低氧条件下的EPC具有毒性作用,能减弱其表达HIF-1α和VEGF.
목적 관찰포도당대내피조세포(EPC)표체저양유도인자1α(HIF-1α)화혈관내피생장인자(VEGF)적영향.방법 재EPC배양체계중가입불동농도포도당,분별재상양(21%양농도)화저양(1%양농도)조건하배양.검측각조HIF-1α급VEGF적기인화단백표체수평.결과 포도당농도상동,저양조표체HIF-1α mRNA고우상양조,VEGF적표체무통계학차이;양농도상동,10mmol/L포도당조EPC표체HIF-1α mRNA고우기여량조,차수착포도당농도증가,VEGF표체축점하강.상양농도하측불도HIF-1α단백표체;저양농도하,10mmol/L포도당조EPC표체HIF-1α최고.결론 고당대저양조건하적EPC구유독성작용,능감약기표체HIF-1α화VEGF.
Objective To observe the effects of various concentrations of glucose on the expression of hypoxiainducible factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF) of endothelial progenitor cells (EPCs). Methods EPCs were cultured in different concentrations of glucose under conditions of normal oxygen environment (21% oxygen) and hypoxia environment (1% oxygen). RT-PCR assays were used for detecting the mRNA level of HIF-1 alpha and VEGF, Western blot for detecting the protein expression of HIF-1 alpha, and ELISA for detecting VEGF secretion. Results The mRNA expression levels of HIF-1 alpha were higher in hypoxia group than in normal oxygen group in the same concentrations of glucose,and much higher under the conditions of same oxygen and 10mmol/L glucose.Under hypoxia condition, the expression levels of HIF-1 alpha were gradually decreased（all P<0.05） with increment of glucose from 5 mmol/L to 10mmol/L and to 33 mmol/L. They were hardly detected under normal hypoxia conditions. The expression level of VEGF was decreased with the increase of glucose in the same concentration of oxygen, but without obvious change in the same concentrations of glucose (P>0.05). Conclusions Highglucose could attenuate the expression of HIF-1 alpha and VEGF of EPCs. This may play an important role in the pathogenesis of diabetic peripheral vascular disease.