Background: The effects of electromagnetic pulse (EMP) radiation on cognitive impairment have attracted much attention, but the mechanism is still unclear. Regulation of brain-derived neurotrophic factor (BDNF) gene expression has been found to promote memory formation and neuronal survival. Isoflurane preconditioning (IP) was reported to have a neuroprotective effect. In this study, we verified the protective effect of IP against brain injury induced by EMP exposure and examined the relation of this effect with BDNF gene regulation.
Methods: Twenty-four hours before EMP exposure, rats were pretreated with 2% inhaled isoflurane for 30 minutes. At 24 hours after EMP injury, the Morris water maze test was carried out. Meanwhile, the other rats were executed and their brain tissues were used for Nissl staining, qRT-PCR, western blot and chromatin immunoprecipitation.
Results: The Morris water maze results showed that 2% IP improved the spatial learning and memory ability of the rats. The Nissl staining results showed 2% of IP alleviated neuronal damage. Also, we detected the mRNA and protein expression of BDNF, and 2% IP significantly increased the expression of BDNF. We also found the expression level of histone deacetylase 2 (HDAC2) was increased and that EMP exposure significantly decreased H3 acetylation, while 2% IP reversed these phenomena, individually, BDNF transcription was activated, and neurogenesis after EMP exposure was alleviated.
Conclusions: Our results suggested that 2% of IP alleviates cognitive impairment induced by EMP exposure in rats. Also, the sustained elevated level of BDNF gene transcription may be an essential mechanism for stimulating neurogenesis because of the increased level of HDAC2-dependent H3 acetylation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.21037/apm-20-1655 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Interactions between epithelial mesenchymal plasticity, barrier dysfunction and innate immune pathways shape the genesis of allergic airway disease.
Expert Rev Respir Med
January 2025
School of Medicine and Public Health, University of Wisconsin Madison, Madison, WI, USA.
Introduction: In genetically predisposed individuals, exposure to aeroallergens and infections from RNA viruses shape epithelial barrier function, leading to Allergic Asthma (AA). Here, activated pattern recognition receptors (PRRs) in lower airway sentinel cells signal epithelial injury-repair pathways leading to cell-state changes [epithelial mesenchymal plasticity (EMP)], barrier disruption and sensitization.
Areas Covered: 1.
Toxin-antitoxin (TA) modules are important mediators of persister cell formation in response to environmental stresses. However, the mechanisms through which persistence is controlled remain poorly understood. , a novel probiotic, can enter a persistent state upon exposure to tetracycline stress.
View Article and Find Full Text PDFDietary arachidonic acid contributes to alleviation of peanut-induced allergy biomarkers in BALB/c, C57BL/6 and CD-1 mice.
Int Immunopharmacol
January 2025
Department of Chemistry, School of Sciences and Engineering, The American University in Cairo, New Cairo, Cairo, Egypt. Electronic address:
Objective: Despite its innumerable, invaluable and unique benefits to human development and welfare, consumption of the omega 6 polyunsaturated fatty acid, arachidonic acid (ARA) generates apprehension due to the association of its metabolites with allergy symptoms. Accordingly, it was deemed important to examine the impact of ARA supplementation on initiation and progress of peanut (PN)-induced allergy in mice of different MHC haplotypes.
Methods: Cohorts of BALB/c, C57BL/6, and outbred CD-1 mice were maintained two weeks before experimentation and until the end of the experiment on mouse food supplemented with equal amounts of milk powder containing 3 or 0 mg ARA/day/mouse, and then exposed to inhalation of 0 or 100 μg/mouse PN flour molecules twice for 4 weeks.
Association between Exposure to Metals during Pregnancy, Childhood Gut Microbiome, and Risk of Intestinal Inflammation in Late Childhood.
Environ Health (Wash)
October 2024
Department of Epidemiology, University of Iowa College of Public Health, Iowa City 52242, Iowa, United States.
Alterations to the gut microbiome and exposure to metals during pregnancy have been suggested to impact inflammatory bowel disease. Nonetheless, how prenatal exposure to metals eventually results in long-term effects on the gut microbiome, leading to subclinical intestinal inflammation, particularly during late childhood, has not been studied. It is also unknown whether such an interactive effect drives a specific subgroup of children toward elevated susceptibility to intestinal inflammation.
View Article and Find Full Text PDFIn vitro and in vivo effects of commercial and environmental microplastics on Unio delicatus.
Ecotoxicology
October 2024
Biology Department, Faculty of Science, Çankırı Karatekin University, Çankırı, Türkiye.
Article Synopsis
- Microplastics (MPs) found in freshwater environments can have toxic effects on freshwater mussels, particularly affecting hemocyte counts and cellular health when exposed to both environmental and commercial types of MPs.
- Experiments showed that high concentrations of MPs led to reduced levels of cellular glutathione and increased signs of oxidative stress in mussels over periods of 7 to 30 days.
- Physical damage to mussel tissues, particularly in gills and digestive glands, was observed, indicating that MPs pose significant ecological health risks to these organisms.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!