The biological effects of electromagnetic pulse (EMP) on the brain have been focused on for years. It was reported that gelatinase played an important role in maintaining brain function through regulating permeability in the blood-brain barrier (BBB). To investigate the effects of EMP on gelatinase of BBB, an in vitro BBB model was established using primary cultured rat brain microvascular endothelial cells (BMVEC), astrocytes and half-contact culture of these cells in a transwell chamber. Cultured supernatant and cells were collected at different time points after exposure to EMP (peak intensity 400 kV/m, rise time 10 ns, pulse width 350 ns, 0.5 pps and 200 pulses). Protein levels of cellular gelatinase MMP-2 and MMP-9, and endogenous inhibitor TIMP-1 and TIMP-2 were detected by Western blot. The activity of gelatinase in culture supernatant was detected by gelatin zymography. It was found that compared with the sham-exposed group, the protein level of MMP-2 was significantly increased at 6 h (p < 0.05), and the protein level of its endogenous inhibitor TIMP-2 did not change after EMP exposure. In addition, the protein levels of MMP-9 and its endogenous inhibitor TIMP-1 did not change after EMP exposure. Gelatin zymography results showed that the activity of MMP-2 in the inner pool and the outer pool of the transwell chamber was significantly increased at 6 h after EMP exposure compared with that of the sham group. These results suggested that EMP exposure could affect the expression and activity of MMP-2 in the BBB model.
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http://dx.doi.org/10.3109/15368378.2016.1140058 | DOI Listing |
Antioxidants (Basel)
December 2024
Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, 46010 Valencia, Spain.
Mercury (Hg) is a highly toxic environmental contaminant that can harm human health, ultimately leading to endothelial dysfunction. Hg toxicity is partially mediated by the exposure of the cell membrane's surface of erythrocytes (RBCs) to phosphatidylserine (PS). In the context of these challenges, hydroxytyrosol, a phenolic compound of olive oil, has the ability to mitigate the toxic effects of Hg.
View Article and Find Full Text PDFExpert 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 PDFInt 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.
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.
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