CAJ | 학술논문

目的：观察小鼠肾积水后缺氧诱导因子‐1（HIF‐1）、血管内皮生长因子（VEGF）、微小RNA（miRNA）‐210在不同时间点的表达变化并探讨其调控机制。方法采用丝线结扎单侧输尿管的方法制备急性完全性单侧肾积水模型（UUO模型），分为假手术对照组和单侧肾积水组，于单侧肾积水后2、5、9、14 d分别颈椎脱臼处死。采用实时荧光定量 PCR检测肾积水后患肾各时间点HIF‐1 mRNA 、VEGF mRNA及miRNA‐210的表达变化，采用Western blot方法检测肾积水后各时间点HIF‐1蛋白的表达变化。结果 HIF‐1 mRNA表达水平在肾积水后表达量逐渐上调（P＜0．05）。VEGF mRNA及miRNA‐210表达水平在肾积水后2 d升高并达到高峰，于UUO后5、9、14 d表达量逐渐下调（P＜0．05）。HIF‐1蛋白表达量逐渐上调。结论肾积水后HIF‐1 mRNA及蛋白表达逐步上调，VEGF mRNA及miRNA‐210表达一过性上调，可能与肾积水后肾皮质被压迫机体对缺氧、缺血产生适应性反应有关。
목적：관찰소서신적수후결양유도인자‐1（HIF‐1）、혈관내피생장인자（VEGF）、미소RNA（miRNA）‐210재불동시간점적표체변화병탐토기조공궤제。방법채용사선결찰단측수뇨관적방법제비급성완전성단측신적수모형（UUO모형），분위가수술대조조화단측신적수조，우단측신적수후2、5、9、14 d분별경추탈구처사。채용실시형광정량 PCR검측신적수후환신각시간점HIF‐1 mRNA 、VEGF mRNA급miRNA‐210적표체변화，채용Western blot방법검측신적수후각시간점HIF‐1단백적표체변화。결과 HIF‐1 mRNA표체수평재신적수후표체량축점상조（P＜0．05）。VEGF mRNA급miRNA‐210표체수평재신적수후2 d승고병체도고봉，우UUO후5、9、14 d표체량축점하조（P＜0．05）。HIF‐1단백표체량축점상조。결론신적수후HIF‐1 mRNA급단백표체축보상조，VEGF mRNA급miRNA‐210표체일과성상조，가능여신적수후신피질피압박궤체대결양、결혈산생괄응성반응유관。
Objective To observe the expression of inducible factor 1(HIF‐1) ,vascular endothelial growth factor(VEGF) and miRNA‐210 and explore the regulatory mechanism after unilateral ureteral occlusion (UUO) .Methods UUO models are made by ligation unilateral ureteral with silk ,and they were divided into sham group and UUO group .All the mice were sacrificed by cer‐vical dislocation after 2 ,5 ,9 and 14 d of UUO .The kidney samples were examined for HIF‐1 mRNA ,VEGF mRNA and miRNA‐210 by quantitative real time reverse transcription polymerase chain reaction (RT‐PCR) ,and HIF‐1 protein by Western blot . Results The expression level of HIF‐1 mRNA was gradually raised after UUO (P<0 .05) ,and compared with the sham group ,the expression level of VEGF mRNA and miRNA‐210 were up regulated after 2 d of UUO and down regulated after 5 ,9 and 14 d of UUO compared with the sham group (P<0 .05);the expression level of HIF‐1 protein increased after UUO compared to the sham group .Conclusion The results of the level of HIF‐1 protein increased and VEGF mRNA and miRNA‐210 were up regulated ,which might be related to the adaptive response of kidney hypoxia and ischemia after UUO .