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

本研究建立了大鼠肾缺血再灌注损伤模型，观察了缺血预处理对肾缺血再灌注损伤的保护作用。我们还试图揭示缺血预处理的潜在机制，发现缺血预处理能有效地减轻肾缺血再灌注对肾小管的损伤。本研究利用基因芯片技术对肾缺血再灌注后肾小管损伤的相关基因表达进行了分析，初步探讨了预处理诱导因子A（Preconditioninginduciblefactor-A，PICA）在肾缺血再灌注损伤中的作用。我们发现，该基因的表达显着增加在mRNA和蛋白质水平的HK 2细胞暴露于缺氧条件下。由于该基因被证明可以调节与内质网应激相关的分子，因此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.