Background: Traumatic brain injury (TBI) is the damage to the brain caused by external blow or jolt to the head or body. TBI secondarily induces cell damage in the hippocampus. This study aimed to investigate effects of resveratrol treatment histological examination and nuclear factor kappa B (NFκB) expression in hippocampus after TBI.
Materials And Methods: Twenty-four rats were assigned to three groups: sham, TBI and TBI + Resveratrol. TBI was conducted by dropping a 50 g weight from a 1-meter height from a tube to the head of animals. 20 mg/kg resveratrol was orally administered to rats after TBI. Blood was collected to measure malondialdehyde (MDA) and glutathione (GSH) contents. Cerebral tissues were processed for histopathology and furtherly for immunohistochemical analysis.
Results: MDA content was significantly increased and GSH value were significantly decreased in TBI group compared to sham group. Resveratrol treatment significantly improved biochemical scores in TBI + Resveratrol group. Normal histological appearance was observed in hippocampal sections of sham group. In TBI group, neurons in hippocampus were degenerated. Their nuclei were pyknotic. Other neurons and supportive neuroglial cells in hippocampal proper and dentate gyrus were also disrupted. Hippocampal proper integrity was lost with vascular dilatation. NFκB was upregulated in hippocampal neurons of TBI group.
Conclusions: Resveratrol treatment alleviated pathologies and downregulated NFκB expression in hippocampus. TBI caused adverse alterations in free radicals' balance system and histological structures of hippocampus. Resveratrol with its antioxidant and anti-inflammatory effects reduced the damage caused by TBI.
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http://dx.doi.org/10.5603/fm.97799 | DOI Listing |
J Neurotrauma
January 2025
Department of Neurosurgery, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Following traumatic brain injury (TBI), inhibition of the Na-K-Cl cotransporter1 (NKCC1) has been observed to alleviate damage to the blood-brain barrier (BBB). However, the underlying mechanism for this effect remains unclear. This study aimed to investigate the mechanisms by which inhibiting the NKCC1 attenuates disruption of BBB integrity in TBI.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Turkey.
Secondary brain damageafter traumatic brain injury (TBI) involves oxidative stress, neuroinflammation, apoptosis, and necroptosis and can be reversed by understanding these molecular pathways. The objective of this study was to examine the impact of tasimelteon (Tasi) administration on brain injury through the nuclear factor erythroid 2-related factor 2 (NRF-2)/heme oxygenase-1 (HO-1) and receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like (MLKL) pathways in rats with TBI. Thirty-two male Wistar albino rats weighing 300-350 g were randomly divided into four groups: the control group, trauma group, Tasi-1 group (trauma + 1 mg/kg Tasi intraperitoneally), and Tasi-10 group (trauma + 10 mg/kg Tasi intraperitoneally).
View Article and Find Full Text PDFCrit Care Med
January 2025
Department of Surgery, Neurology and Neurosurgery Unit, Federal University of Góias, Góias, Brazil.
Objectives: Balancing oxygen requirements, neurologic outcomes, and systemic complications from transfusions in traumatic brain injury (TBI) patients is challenging. This review compares liberal and restrictive transfusion strategies in TBI patients.
Data Sources: Electronic databases were searched from inception to October 2024.
<b>Background and Objective:</b> It is well documented that Whole Genome Sequencing (WGS) has recently used to explore new resistance patterns and track the dissemination of extensive and pan drug-resistant microbes in healthcare settings. This article explores the link between traumatic infections caused by road traffic accidents (RTAs) leading to coma and the development of chest infections caused by extensively drug-resistant (XDR) <i>Klebsiella pneumoniae</i> and <i>Pseudomonas aeruginosa</i>. <b>Materials and Methods:</b> The study was carried out from March to December 2022 which included a 45-year-old male patient admitted to the ICU of Al Ramadi Teaching Hospitals following a severe RTA that resulted in a TBI and subsequent coma.
View Article and Find Full Text PDFMethodsX
June 2025
Neurorehabilitation and Neuromodulation Laboratory, Department of Physiological Sciences, Federal University of Espírito Santo, City of Vitória, ES, Brazil.
Traumatic brain injury (TBI) is a global public health condition that causes cognitive and behavioral deficits. This protocol assesses the potential of quantitative electroencephalogram (EEG) biomarkers, associated with inflammatory indicators, to predict mortality and functional recovery in patients with severe TBI. Through continuous monitoring and analysis of abnormal brain activity patterns, the protocol aims to personalize therapeutic interventions and improve patient quality of life.
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