Neuroprotective Effects of Sildenafil on Traumatic Brain Injury in an Experimental Rat Model

Abstract

Abstract Objective Not only primary injuries, secondary injuries such as posttraumatic biochemical cascades, ischemia, and hypoxia also affect the morbidity and mortality of traumatic brain injury (TBI). Sildenafil released the vasodilatation by relaxing the smooth muscle of the systemic artery and vein. Also, the effects of sildenafil are evidenced in multiple sclerosis, Alzheimer's disease, and memory loss as a part of experimental studies. Sildenafil decreases oxidative stress by increasing the cGMP level. We aimed to examine the protective effects of sildenafil on TBI with histopathological and biochemical parameters. Method 21 Sprague–Dawley rats were separated into three groups (n = 7). “The weight drop injury model,” which was described by Marmou, was used for the head injury. Group 1: nontraumatic sham group, Group 2: nontreated TBI group, Group 3: sildenafil (100 mg/kg) treated TBI group. The whole brain and serum were collected for histopathological and biochemical study. The histopathological sections were examined under a light microscope. Results On comparison of total antioxidant status (TAS), total oxidant status (TOS), nitric oxide (NO), and plasma nitrite/nitrate (PNOx) between groups, NO level was significantly high in group 3 (p = 0.013). Even though the TAS level was significantly high in group 3 (p = 0.02), there were no significant differences in TOS level in groups (p = 0.225). Disappearing Nissle granules occurred in a pyknotic situation in the cell nucleus, and acidophilic staining in neuron cells, which describe the neuron degeneration observed in the trauma group. The neuron degeneration markers were not seen in the sildenafil-treated trauma group. Conclusion Our study has shown that sildenafil decreases the oxygen radicals and affects the recovery of experimental TBI in rats.