Affiliation:
1. University of Health Sciences, Kartal Dr. Lutfi Kırdar Education and Research Hospital, Department of Neurosurgery
2. Sivas Numune Hospital, Department of Neurosurgery
Abstract
Objective: Sesamol is a powerful antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective chemical. This study aimed to investigate the histopathological effects of sesamol in a rat traumatic brain injury (TBI) model. Material and Methods: Thirty-two male rats were divided into the following four groups: control, trauma, vehicle, and sesamol. All groups were subjected to TBI, and immediately after trauma saline and sesamol (100 mg/kg) were administered intraperitoneally to the vehicle and sesamol groups, respectively. At 24th hour of TBI, brain samples were collected, and histomorphological investigation of brain parenchyma was performed using electron and light microscopy. Results:On histopathological investigation, TBI induced brain injury was lesser than trauma and vehicle groups in the sesamol group. Compared to the trauma group, in the sesamol group there was less perivascular region edema. The neuronal processes of the sesamol group also displayed less intracellular edema and vacuoles. Conclusion:The results of the current study revealed for the first time that sesamol exhibits neuroprotective effects against TBI.
Publisher
Kirikkale Universitesi Tıp Fakultesi Dergisi
Reference31 articles.
1. Acosta SA, Tajiri N, Shinozuka K, Ishikawa H, Grimmig B, Diamond DM, et al. Long-term upregulation of inflammation and suppression of cell proliferation in the brain of adult rats exposed to traumatic brain injury using the controlled cortical impact model. PLoS One. 2013;8(1):e53376.
2. Salehi A, Zhang JH, Obenaus A. Response of the cerebral vasculature following traumatic brain injury. J Cereb Blood Flow Metab. 2017;37(7):2320-39.
3. Lozano D, Gonzales-Portillo GS, Acosta S, de la Pena I, Tajiri N, Kaneko Y, et al. Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities. Neuropsychiatr Dis Treat. 2015;11:97-106.
4. Perez-Polo JR, Rea HC, Johnson KM, Parsley MA, Unabia GC, Xu G, et al. Inflammatory consequences in a rodent model of mild traumatic brain injury. J Neurotrauma. 2013;30(9):727-40.
5. Pop V, Badaut J. A neurovascular perspective for long-term changes after brain trauma. Transl Stroke Res. 2011;2(4):533-45.