Traumatic brain injury (TBI) is a severe damage to the head that causes vasogenic edema resulted from disruption of the blood-brain barrier (BBB). Sonic hedgehog (Shh) is a hedgehog family protein, which exerts protective effects for cerebrovascular and neuronal cells after brain damages via the patched-1-smoothened-Gli signaling pathway. Thus, we investigated effects of the Shh signaling for TBI-induced vasogenic edema in model mice. The TBI model was determined by inflicting a fluid percussion injury (FPI) in the mouse cerebrum. Vasogenic edema was assessed by the Evans blue extravasation into the brain tissue and the increased brain water content. Evans blue extravasation and brain water content were increased by FPI, whereas repeated intracerebroventricular administration of recombinant Shh (0.1, 1, 10 μg/day) from 3 hours to 3 days after FPI reduced Evans blue extravasation and the brain water content in the injured cerebrum. On the other hands, Jervine, a smoothened antagonist aggravated these conditions. Administration of Shh increased expression levels of tight junction proteins and angiopoietin-1, a vascular protective factor in the injured cerebrum after FPI. These results suggest that Shh signaling alleviates TBI-induced vasogenic edema by increasing tight junction proteins and angiopoietin-1.