151. Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?
- Author
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Mohammad Khaksari, Mohammad Amin Rajizadeh, Mohammad Abbas Bejeshk, Zahra Soltani, Sina Motamedi, Fatemeh Moramdi, Masoud Islami, Shahriyar Shafa, and Sepehr Khosravi
- Subjects
Angiotensin II receptor ,Blood-brain barrier ,Brain edema ,Brain injury ,Candesartan ,Intracranial pressure ,Lipid peroxidation ,Medicine - Abstract
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.
- Published
- 2018
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