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缺血后处理对缺血再灌注损伤大鼠肾脏HIF-1α的影响
引用本文:李苏童,王汉民,李嫚,刘广厚,何丽洁,陈光磊,张鹏. 缺血后处理对缺血再灌注损伤大鼠肾脏HIF-1α的影响[J]. 中国血液净化, 2008, 7(5): 266-269
作者姓名:李苏童  王汉民  李嫚  刘广厚  何丽洁  陈光磊  张鹏
作者单位:第四军医大学西京医院肾脏科,西安710032
摘    要:目的 观察缺血后处理对缺血再灌注损伤(IRI)大鼠肾脏缺氧诱导因子-1α(HIF-1α)表达的影响。方法 将72只成年SD大鼠随机分为假手术组(S组)、缺血再灌注组(IR组)、缺血后处理组(IPO组),每组24只。S组结扎右肾动脉,暴露左肾45min后关闭腹腔;IR组结扎右肾动脉并完全阻断左侧肾动脉45min后恢复血流;IPO组在IR模型的基础上,恢复血流前给予反复10次20s供血20s缺血处理。每组分别在造模后0.5h、1h、3h、6h、12h、24h、48h、72h留取血和肾组织标本,检测血肌酐和血尿素氮,并对肾组织行免疫组化染色和单言评分;Western blot检测HIF-1α的表达强度。结果 HIF-1α主要在小管上皮细胞中表达,肾小球中未发现阳性染色。各组HIF-1α表达情况:与S组相比IR组HIF-1α在1h表达开始显著升高,6h达到高峰,12h开始下降。而IPO组HIF-1α在3h表达开始升高,6h达到高峰,且高峰水平显著高于IR组,24h后HIF-1α开始下降,48h其表达水平与IR组差异无显著性。结论 缺血后处理能增加缺血再灌注损伤大鼠肾脏HIF-1α表达并延长其表达高峰时间,从而减轻缺血缺氧对肾脏的损伤。

关 键 词:缺血再灌注  缺血后处理  HIF-1α  肾脏
修稿时间:2008-01-29

Effect of ischemic postconditioning on expression of HIF-1α in the kidney after ischemia-reperfusion injury in rats
LI Su-tong,WANG Hai-min,LI Man,LIU Guang-hou,HE Li-jie,CHEN Guang-lei,ZHANG Peng. Effect of ischemic postconditioning on expression of HIF-1α in the kidney after ischemia-reperfusion injury in rats[J]. Chinese Journal of Blood Purification, 2008, 7(5): 266-269
Authors:LI Su-tong  WANG Hai-min  LI Man  LIU Guang-hou  HE Li-jie  CHEN Guang-lei  ZHANG Peng
Affiliation:. Neph- rology( Department, Xijing Hospital, Fourth Military Medical University, Xi' an 710032, China )
Abstract:Objective To investigate the effect of ischemic postconditioning on HIF-1α expression in the kidney after ischemic-reperfusion injury in rats. Methods Seventy-two Sprague-Dawley rats were randomized into 3 groups: sham operation group (S group), ischemia-reperfusion group (IR group) and ischemic postconditioning group (IPO group). For rats in S group, we ligated the right renal artery, and separated and exposed the left kidney for 45min. For those in IR group, we ligated the right renal artery, and clamped the left renal artery for 45min. For those in IPO group, we also ligated the right renal artery and clamped the left renal artery for 45min, but we then sequentially loosed the clamp for 20sce and closed the clamp for 20sec for 10 cycles before recovery of the left kidney from ischemia. After the operation for 0.5h, lh, 3h, 6h, 12h, 24h, 48h and 72h, rats were sacrificed, plasma creatinine and blood urea nitrogen were measured, and kidney samples were examined for HIF-1α by immunochemistry and western blotting. Results HIF-1α expressed in tubular epithelia but not in glomeruli. In IR group, renal HIF-1α expression increased at lh, reached peak at 6h, and began to decrease at 12h. In IPO group, renal HIF-1α expression increased at 3h, reached peak at 6h, and began to decrease at 24h. The peak HIF-1α value was higher in IPO group than in IR group. At 48h, renal HIF-1α value was similar between IR and IPO groups. Conclusion Ischemic postconditioning increases HIF-1α expression and elongates its peak expression period in the kidney after ischemia-reperfusion injury. These changes of renal HIF-1α may facilitate the recovery of kidney from ischemia-reperfusion injury.
Keywords:Ischemia-reperfusion  Ischemic postconditioning  HIF-1α  Kidney
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