The term mitophagy is coined to describe the selective removal of mitochondria by autophagy but the process itself is still contentious, especially in the early brain injury following subarachnoid hemorrhage (SAH). In the present study, we investigated the role of mitophagy following 48hours after SAH injury in rats. Specifically evaluating whether through an Voltage‐dependent anion channels(VDACs) interacting with microtubule‐associated protein 1 light chain3(LC3), mitophagy could orchestrate the induction of apoptotic and necrotic cell death in neurons. A VDAC1siRNA and a activitor Rapamycian(RAPA) were engaged. One hundred and twelve male Sprague‐Dawley rats were randomly divided into 4 groups: Sham, SAH, SAH+ VDAC1siRNA, and SAH+RAPA. Outcomes measured include mortality rate, brain edema, BBB disruption, and neurobehavioral testing. We also used western blotting techniques to measure the expressions of key mitophagic/autophagic proteins and pro‐apoptotic protein such as ROS, VDAC1, LC‐3II and Caspase‐3. Rapamycin treatment significantly alleviated the mortality rate, cerebral edema, neurobehavioral deficits, and apoptotic and necrotic cell death in neurons as observed by histology following SAH injury. However, VDAC1siRNA deteriorated the brain injury on the basic injury of SAH. Immunohistochemical staining and western blot analysis demonstrated an increased expression of VDAC1, LC3, and a decrease of ROS and Caspase‐3 followed by rapamycin administration. In conclusion, this study showed that mitophagy following the SAH injury may in fact play a significant role in the neuroprotection following SAH and its mediation may be through attenuating the apoptosis and necrosis molecular pathway. This translates a preservation of functional integrity and an improvement in mortality.