Objective To examine the level of mitochondrial autophagy in nerve cells after cerebral ischemiareperfusion and to explore the relationship between cerebral ischemia-reperfusion injury and mitochondrial autophagy in mice. Methods Seventy C57BL/6J mice were divided randomly into a blank group, sham operation group, and ischemiareperfusion group. Body weight and Zea Longa score were recorded daily. After rapid head decapitation, infarcted side brain tissue was taken for detection. 2,3,5-triphenyte-trazolium chloride detection, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling, transmission electron microscopy, Western blot and quantitative polymerase chain reaction detection at the 1st, 3rd, and 7th day. Results After modeling, the Zea Longa score decreased continuously, the relative cerebral infarction area increased, and the pathological changes of cerebral ischemia and the proportion of neuronal apoptosis were all aggravated on day 3 and alleviated on day 7. Structural changes in the mitochondria and the presence of autophagy lysosomes were observed by electron microscopy at all three time points. Protein expression of P62 decreased continuously (P< 0. 05), the LC3Ⅱ/ LC3Ⅰ ratio increased continuously(P<0. 05), expression levels of Caspase3 and cytC protein increased (P<0. 05), and mRNA expression levels of all factors increased (P<0. 05). Conclusions Mitochondrial autophagy was continuously activated after ischemia-reperfusion, but reperfusion injury was not alleviated until 3 days after reperfusion.