Objective      To determine the effects of sevoflurane preconditioning on function of autophagy in lung ischemiareperfusion(I/R) injury in rats.   Methods       A lung I/R injury model in rats was established by clamping of the left hilum after thoracotomy.A total of 75 healthy adult male Sprague-Dawley (SD) rats (SPF grade) were randomly divided into 5 groups（n=15）: sham operation group（Sham）

ischemia-reperfusion group（I/R）

sevoflurane preconditioning group（SEVO）

LY294002（LY

PI3K inhibitor） group

sevoflurane preconditioning+LY294002 group（SEVO+LY）. After 1 h of ischemia and 120 min of reperfusion，the rats were executed and the left lung tissue were harvested for wet-dry weight （W/D）measurement. Western blotting was used to detect the expression of Beclin-1

LC3Ⅱ/Ⅰ

P62 and p-PI3K.  Results       Compared with the Sham group

I/R group developed severe lung edema (P0.05)

and had increased level of autophagy and its related protein expression of Beclin1

LC3Ⅱ/Ⅰ

P62 (P0.05). The pulmonary injury and increased protein expression found in I/R group were significantly reduced in SEVO group (P0.05). Only p-PI3K expression was significantly increased in the SEVO group than the I/R group （P0.05）.There were no significant differences between LY group and I/R group in these respects（P0.05）. In SEVO+LY group

pulmonary injury was aggravated.The expression of Beclin-1

LC3Ⅱ/Ⅰ

P62 was up-regulated and p-PI3K level was remarkably decreased compared with SEVO group（P0.05）. Conclusion       The results demonstrated that autophagy was involved in the lung I/R pathophysiological process. Sevoflurane preconditioning can protect the lung I/R injury in rats

which is likely related to activation of PI3K signaling transduction and restoration of autophagic flux，at last reducing autophagic cell death.