ArticleIranian journal of basic medical sciences2018
Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?
Article in Iranian journal of basic medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Ang II-mediated effects on BBB integrity in psychiatric and neurological disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2026Review
- Combination Therapy of Estrogen and Progesterone Attenuates Behavioral Impairments and Autophagy via circLrp1b/miR-27a-3p/Dram2 Pathway After Traumatic Brain Injury.Molecular neurobiology · 2025Article
- Candesartan Mitigates Perioperative Neurocognitive Disorders by Modulating Hypertension-Linked Neuroinflammatory Factor.Neurochemical research · 2025Article
- Optimal Timing of Exercise for Enhanced Learning and Memory: Insights From CA1 and CA3 Regions in Traumatic Brain Injury Model in Male Rats.Brain and behavior · 2025Article
- Evaluation of canine adipose-derived mesenchymal stem cells for neurological functional recovery in a rat model of traumatic brain injury.BMC veterinary research · 2024Article
- Interaction of estradiol and renin-angiotensin system with microRNAs-21 and -29 in renal fibrosis: focus on TGF-β/smad signaling pathway.Molecular biology reports · 2024Review
- The Role of Inhaled Estradiol and Myrtenol, Alone and in Combination, in Modulating Behavioral and Functional Outcomes Following Traumatic Experimental Brain Injury: Hemodynamic, Molecular, Histological and Behavioral Study.Neurocritical care · 2023Article
- Relationship between in-hospital angiotensin converting enzyme inhibitors and Angiotensin receptor blockers administration and delirium in the cardiac ICU.Hospital practice (1995) · 2023Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- The Effect of Oral Mucosal Mesenchymal Stem Cells on Pathological and Long-Term Outcomes in Experimental Traumatic Brain Injury.BioMed research international · 2022Article
- Manifestation of renin angiotensin system modulation in traumatic brain injury.Metabolic brain disease · 2021Review
- The Changes of Brain Edema and Neurological Outcome, and the Probable Mechanisms in Diffuse Traumatic Brain Injury Induced in Rats with the History of Exercise.Cellular and molecular neurobiology · 2020Article
- Can Mesenchymal Stem Cells Act Multipotential in Traumatic Brain Injury?Journal of molecular neuroscience : MN · 2020Review
- Losartan Treatment Could Improve the Outcome of TBI Mice.Frontiers in neurology · 2020Article
- The Effect of Candesartan Alone and Its Combination With Estrogen on Post-traumatic Brain Injury Outcomes in Female Rats.Frontiers in neuroscience · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesNeuroprotection 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
methodsMale 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.
resultsBrain 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.
conclusionThe 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.
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