%0 Journal Article %T Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury? %J Iranian Journal of Basic Medical Sciences %I Mashhad University of Medical Sciences %Z 2008-3866 %A Khaksari, Mohammad %A Rajizadeh, Mohammad Amin %A Bejeshk, Mohammad Abbas %A Soltani, Zahra %A Motamedi, Sina %A Moramdi, Fatemeh %A Islami, Masoud %A Shafa, Shahriyar %A Khosravi, Sepehr %D 2018 %\ 06/01/2018 %V 21 %N 6 %P 615-620 %! Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury? %K Angiotensin II receptor %K Blood-brain barrier %K Brain edema %K Brain injury %K Candesartan %K Intracranial pressure %K Lipid Peroxidation %R 10.22038/ijbms.2018.26586.6512 %X Objective(s): Neuroprotection is created following the inhibition of angiotensin II type 1 receptor (AT1R). Therefore, the purpose of this research was examining AT1R blockage by candesartan in diffuse traumatic brain injury (TBI). Materials and Methods: Male rats were assigned into sham, TBI, vehicle, and candesartan groups. Candesartan (0.3 mg/kg) or vehicle was administered IP, 30 min post-TBI. Brain water and Evans blue contents were determined, 24 and 5 hr after TBI, respectively. Intracranial pressure (ICP) and neurologic outcome were evaluated at -1, 1, 4 and 24 hr after TBI. Oxidant index [malondialdehyde (MDA)] was determined 24 hr after TBI.Results: Brain water and Evans blue contents, and MDA and ICP levels increased in TBI and vehicle groups in comparison with the sham group. Candesartan attenuated the TBI-induced brain water and Evans blue contents, and ICP and MDA enhancement. The neurologic score enhanced following candesartan administration, 24 hr after TBI.Conclusion: The blockage of AT1R may be neuroprotective by decreasing ICP associated with the reduction of lipid peroxidation, brain edema, and blood-brain barrier (BBB) permeability, which led to the improvement of neurologic outcome. %U https://ijbms.mums.ac.ir/article_10694_0a2ad7a22d187d10470a8d705e98ff92.pdf