Ischemic preconditioning (IPC) is a brief episode of ischemia/reperfusion (I/R) that protects the brain from the damage induced by subsequent prolonged ischemia. It confers both early and delayed tolerance over a period of a few minutes to days (1). Rho-kinases (ROCK) are serine-threonine kinases that critical in cell migration and survival, activation of ROCK pathway was observed in cerebral ischemia (2). The aim of the present work was to study the neuroprotective potential of IPC. 24 adult male Wistar rats (150-250g) were divided into three groups 8 rats in each; first group was sham-operated and served as a control, I/R group of rats subjected to 30 minutes of left common carotid artery occlusion followed by 24-hour of reperfusion, anesthesia was induced by ether inhalation and maintained by thiopental sodium (2.5mg/kg) (3). IPC group were treated with three episodes of 5-minutes of ischemia with 10 minutes of reperfusion in between, followed by 30 minutes of ischemia and then allowed for reperfusion for 24-hours. Neurobehavioral assessments were evaluated (4); ROCK using enzyme-linked immunosorbent assay was measured in affected cerebral hemisphere. Values are means ± S.E.M, compared by ANOVA. The IPC group showed a significant improvement in neurological deficit (16.9±0.50) compared to both I/R and control groups (12.798±0.689, 17.50±0.707, respectively P <0.001). In I/R group ROCK was significantly increased (1.13±0.17 ng/mg protein, P <0.001) as compared to IPC group, but not to control group (p=0.198). Rats subjected to IPC demonstrated a significant decrease in ROCK level (0.39±0.19 ng/mg protein, P <0.001) to both control (1.3±0.30 ng/mg protein) and I/R group. So IPC affords protection against a subsequent I/R challenge. We established an Ischemic preconditioning model in which rats showed improvement in neurological deficits and decreased ROCK level following transient focal cerebral ischemia reperfusion in rats.