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      The effect of rosmarinic acid on deformities occurring in brain tissue by craniectomy method. Histopathological evaluation of IBA-1 and GFAP expressions

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          Abstract Purpose To investigate the role of Rosmarinic acid (RA) in the prevention of traumatic brain injury and the immunohistochemical analysis of IBA-1 and GFAP expressions. Methods Healthy male rats were randomly divided into 3 groups consisting of 10 rats. Groups were as follows; control group, traumatic brain injury (TBI) group, and TBI+RA group. After traumatic brain injury, blood samples were taken from the animals and analyzed with various biochemical markers. And then IBA-1 and GFAP expressions were evaluated immunohistochemically. Results Significant results were obtained in all biochemical parameters between groups. Immunohistochemical sections showed IBA-1 not only in microglia and macrophage activity but also in degenerative neurons in blood vessel endothelial cells. However, GFAP reaction and post-traumatic rosmarinic acid administration showed positive expression in astrocytes with regular structure around the blood vessel. Conclusion Rosmarinic acid in blood vessel endothelial cells showed that preserving the integrity of astrocytic structure in the blood brain barrier may be an important antioxidant.

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          Malondialdehyde determination as index of lipid peroxidation.

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            The neuropathology and neurobiology of traumatic brain injury.

            The acute and long-term consequences of traumatic brain injury (TBI) have received increased attention in recent years. In this Review, we discuss the neuropathology and neural mechanisms associated with TBI, drawing on findings from sports-induced TBI in athletes, in whom acute TBI damages axons and elicits both regenerative and degenerative tissue responses in the brain and in whom repeated concussions may initiate a long-term neurodegenerative process called dementia pugilistica or chronic traumatic encephalopathy (CTE). We also consider how the neuropathology and neurobiology of CTE in many ways resembles other neurodegenerative illnesses such as Alzheimer's disease, particularly with respect to mismetabolism and aggregation of tau, β-amyloid, and TDP-43. Finally, we explore how translational research in animal models of acceleration/deceleration types of injury relevant for concussion together with clinical studies employing imaging and biochemical markers may further elucidate the neurobiology of TBI and CTE. Copyright © 2012 Elsevier Inc. All rights reserved.
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              A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics.

              This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.
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                Author and article information

                Journal
                acb
                Acta Cirurgica Brasileira
                Acta Cir. Bras.
                Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (São Paulo, SP, Brazil )
                0102-8650
                1678-2674
                2020
                : 35
                : 4
                : e202000406
                Affiliations
                [2] Diyarbakır orgnameDicle University orgdiv1Faculty of Medicine orgdiv2Department of Histology and Embryology Turkey
                [1] Diyarbakır orgnameDicle University orgdiv1Faculty of Medicine orgdiv2Department of Neurosurgery Turkey
                [3] Diyarbakır orgnameDicle University orgdiv1Faculty of Medicine orgdiv2Department of Anatomy Turkey
                Article
                S0102-86502020000400200 S0102-8650(20)03500400200
                10.1590/s0102-865020200040000006
                d0cd6add-cf41-48b4-bdea-8071a761eac5

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 04 March 2020
                : 06 December 2019
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 40, Pages: 0
                Product

                SciELO Brazil

                Self URI: Full text available only in PDF format (EN)
                Categories
                Original Articles

                Glial Fibrillary Acidic Protein,Rats,Brain Injuries, Traumatic,Rosmarinic Acid

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