肾小管上皮细胞损伤是急性肾损伤（AKI）的中心环节。受损伤肾小管上皮细胞线粒体含量减少及功能受损致ATP合成减少，使得小管上皮细胞损伤进一步加重，纠正细胞ATP缺乏则可望减轻小管上皮细胞损伤。促进小管上皮细胞线粒体生成与调控参与氧化磷酸化（OXPHOS）复合物含量及活性可以增加细胞ATP合成以缓解细胞ATP 缺乏。AMPK作为一种调控能量代谢的蛋白激酶，可通过PGC-1α及线粒体内蛋白激酶调控线粒体生成与OXPHOS复合物含量及活性。我们的预实验结果显示，激活AMPK能够减轻肾小管上皮细胞损伤以改善AKI大鼠肾功能。据此我们提出是否AMPK激活可通过调控线粒体生成及ATP合成以保护AKI肾小管上皮细胞？本研究将构建缺血/再灌注体内及体外模型，应用分子生物学、线粒体蛋白组学及高效液相色谱方法，探讨AMPK-PGC-1α调控线粒体生成及线粒体ATP合成以保护肾小管上皮细胞的机制。

The central aspect of AKI is the injury of renal tubular epithelial cells. Decrease of mitochondria quantity and scarcity of ATP are considered the typical characteristic of AKI. Normalization of ATP level may improve the injured renal tubular epithelial cells. The scarcity of ATP can be solved by promoting energy synthesis of mitochondria. Up-regulation of mitochondria quantity and enhancement of the activity of OXPHOS complexes may increase the ATP level. AMPK can act on the two aspects through the activation of PGC-1α. The pre-experiments of our team showed that AMPK activator could increase the quantity of mitochondria, decrease the apoptosis of renal tubular epithelial cells, and preserve the renal function. In our study, we will investigate the relationship between AMPK- PGC-1α and the synthesis of ATP in the in vivo and in vitro model. We will also study the mechanism of renal tubular epithelial cell protection under the activation of AMPK- PGC-1α.