Objective Based on the regulation of mitochondrial function through HIF-1α, to explore the effects of dexmedetomidine on the neurological function of rats with ischemic stroke. Methods 48 SD rats were randomly divided into Sham group, Ischemia stroke group, Dexmedetomidine group, and Dexmedetomidine+YC-1 group. Longa method was applied to construct cerebral ischemia / reperfusion model in rats except for Sham group, during which dexmedetomidine (50 μg/kg) or YC-1 (5mg/kg) was injected intraperitoneally. After 24 hours, neurological function and the cerebral infarction volume were evaluated, and then the brains were taken and mitochondria were extracted to detect the activity of mitochondrial membrane potential and mitochondrial respiratory chain complexes. Finally, the levels of ROS, GSH and ATP were detected by the kit, and HIF-1α was detected by Western blot. Results Rats in Ischemia stroke group appeared decreases in the neurological score and cerebral infarction. Compared with Ischemia group, dexmedetomidine significantly increased the neurological scores of rats and reduced the proportion of cerebral infarction volume. In addition, dexmedetomidine up-regulated the level of mitochondrial membrane potential and increased the activity of mitochondrial respiratory chain complex Ⅰ/Ⅱ/Ⅲ. At the same time, the expression of HIF-1α in brain of the dexmedetomidine group was significantly increased, and the level of ROS decreased while the level of GSH and ATP increased significantly. However, the expression of HIF-1α in the brain tissue of rats in the dexmedetomidine+YC-1 group significantly reduced, and the mitochondrial membrane potential significantly reduced, the activity of respiratory chain complexes reduced as well. In the end, rats showed an increase in neurological score and an increase in the proportion of cerebral infarction volume. Conclusion Dexmedetomidine improves mitochondrial function by up-regulating the expression of HIF-1α, thereby reducing oxidative stress, reducing cerebral infarction areas, and ultimately exerting neuroprotective effects.