Objective To investigate the effects of edaravone on the JNK signaling pathway and neuronal autophagy in the hippocampus in rats with subarachnoid hemorrhage (SAH).Methods A total of 40 adult male Sprague-Dawley rats were equally and randomly divided into four groups: sham-operation group, SAH model group, edaravone group, and SP600125 (JNK inhibitor) group. The SAH model rats were prepared using the modified intracranial arterial puncture method; the sham-operation group was treated as well, but the artery was not catheterized. The rats in the SP600125 group received an injection of SP600125 solution (3 μg/μl, 10 μl) at the lateral ventricle through a stereotaxic apparatus at 30 minutes before SAH modeling. The rats in the edaravone group received an intraperitoneal injection of edaravone (5 mg/kg) after SAH modeling and once again after 12 hours. All rats were sacrificed after 24 hours. HE staining was used to observe the changes in the morphology and number of hippocampal neurons, and immunohistochemical staining and Western blot were used to evaluate the changes in the expression of Beclin-1, LC3-II protein, and p-JNK protein.Results In the sham-operation group, the brain tissues remained integral in structure and the number and morphology of hippocampal neurons remained normal. In the SAH model group, hippocampal neurons mostly appeared disordered and triangular-pyramidal; the number of surviving cells was significantly lower than that in the sham-operation group (P<0.05); the expression of Beclin-1, LC3-II protein, and p-JNK protein was significantly higher than that in the sham-operation group (P<0.05). Compared with the SAH model group, the edaravone group and the SP600125 group had a significantly lower death rate of hippocampal neurons (P<0.05), a significantly higher number of neurons with normal morphology (P<0.05), and significantly lower expression of Beclin-1, LC3-II protein, and p-JNK protein (P<0.05).Conclusions Edaravone can reduce the expression of Beclin-1 and LC3-II protein in the hippocampal neurons of SAH rats and alleviate the early brain injury after SAH, which may be dependent on the JNK signaling pathway.