Despite remarkable advances in epilepsy research, prevention and reversal of cognitive deficits following epilepsy remain a challenge. It was reported that the Rho kinase (ROCK) inhibitor fasudil hydrochloride (FH) could improve cognitive deficits in animal models of Alzheimer’s disease (AD). Thus the aim of the present study was to determine whether FH-mediated inhibition of the effects of ROCK signaling could improve seizure-induced cognitive deficits in male rats and to elucidate the underlying mechanisms. Western blotting analysis showed up-regulation of phosphorylated RhoA (p-RhoA) expression, and indicated activation of Rho/ROCK signaling after status epilepticus (SE). The Morris water maze (MWM) test was used to analyze learning-memory ability. HE staining, immunofluorescence staining with anti-neuronal nuclei (NeuN) and anti-neurofilament proteins 200 kD (NF200), transmission electron microscopy (TEM), and quantitative analysis of NeuN and synaptophysin (SYP) by western blotting were performed to observe alterations in neurons, axons, and synapses in the hippocampi. Electroencephalogram (EEG) monitoring was used to record electrophysiological activities after SE. Our results indicated that treatment with FH could ameliorate cognitive dysfunction by reducing neuron, axon, and synapse damage, and mitigating EEG discharges, suggesting various roles for the Rho/ROCK signaling pathway in the pathological processes of brain damages following SE induced by lithium-Pilocarpine. The Rho/ROCK signaling pathway is therefore a potential therapeutic target for the prevention or reversal of cognitive dysfunction caused by epilepsy.