A study to examine the renal protective effect and the remote effect of ischemic preconditioning for renal ischemia/reperfusion injury

建立大鼠肾缺血/再灌注模型，观察缺血预适应对肾缺血/再灌注损伤的保护作用。我们还试图揭示缺血预适应的潜在机制。我们发现，缺血预适应可以有效地减轻肾缺血/再灌流对含尿小管的损伤。根据基因芯片的综合基因表达分析结果，我们重点研究了预适应诱导因子-A(PICA)作为与肾缺血/再灌流后含尿小管损伤相关的因子。我们发现，当HK2细胞暴露在低氧条件下时，该基因在mRNA和蛋白水平的表达明显上调。由于该基因被证明调控与内质网应激相关的分子，我们正在分析该基因与内质网应激的关系。

We made a rat model of renal ischemia/reperfusion and examined the effectiveness of ischemic preconditioning for preventing renal ischemia/reperfusion injury. We also sought to reveal the underlying mechanism of ischemic preconditioning.We found that ischemic preconditioning could efficiently reduce the damage for uriniferous tubules by renal ischemia/reperfusion. We focused on Preconditioning inducible factor-A (PICA) as a factor that is related to the damage of uriniferous tubules after renal ischemia/reperfusion according to the results of comprehensive gene expression analyses with DNA microarray. We found that the expression of this gene was conspicuously elevated at mRNA and protein level in HK2 cells when the cells were exposed to the hypoxic condition. As this gene was shown to regulate the molecules that are related to endoplasmic reticulum stress, we are in progress for analyzing the relationship of this gene and endoplasmic reticulum stress.