Significant effort has been focused on reducing neuronal damage from post-traumatic brain injury (TBI) inflammation and blood-brain barrier (BBB)-mediated edema. The orexigenic hormone ghrelin decreases inflammation in sepsis models, and has recently been shown to be neuroprotective following subarachnoid hemorrhage. We hypothesized that ghrelin modulates cerebral vascular permeability and mediates BBB breakdown following TBI. Using a weight-drop model, TBI was created in three groups of mice: sham, TBI, and TBI/ghrelin. The BBB was investigated by examining its permeability to FITC-dextran and through quantification of perivascualar aquaporin-4 (AQP-4). Finally, we immunoblotted for serum S100B as a marker of brain injury. Compared to sham, TBI caused significant histologic neuronal degeneration, increases in vascular permeability, perivascular expression of AQP-4, and serum levels of S100B. Treatment with ghrelin mitigated these effects; after TBI, ghrelin-treated mice had vascular permeability and perivascular AQP-4 and S100B levels that were similar to sham. Our data suggest that ghrelin prevents BBB disruption after TBI. This is evident by a decrease in vascular permeability that is linked to a decrease in AQP-4. This decrease in vascular permeability may diminish post-TBI brain tissue damage was evident by decreased S100B.
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http://dx.doi.org/10.1089/neu.2011.2053 | DOI Listing |
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Institute of Experimental Medicine, Almazov National Medical Research Centre, 15B Parkhomenko Street, 194021 Saint Petersburg, Russia.
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase (MLCK)-dependent endothelial hyperpermeability, which is considered a preventable cause of reperfusion injury. In the present study, a single intravenous injection of MLCK peptide inhibitor PIK7 (2.
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Department of Anatomy and Embryology, Iuliu Hatieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
The streptozotocin-induced rat model of diabetic retinopathy presents similarities to the disease observed in humans. After four weeks following the induction of diabetes, the rats experience vision impairment. During this crucial four-week period, significant changes occur, with vascular damage standing out as a clinically significant factor, alongside neovascularization.
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Department of Biology, Concordia University, Montreal, QC H4B 1R6, Canada.
Gene therapy targeting ischemic heart disease is a promising therapeutic avenue, but it is mostly restricted to viral-based delivery approaches which are limited due to off-target immunological responses. Focused ultrasound presents a non-viral, image-guided technique in which circulating intravascular microbubble contrast agents can reversibly enhance vascular permeability and gene penetration. Here, we explore the influence of flow rate on the microbubble-assisted delivery of miR-126, a potent pro-angiogenic biologic, using a custom acoustically coupled pressurized mesenteric artery model.
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Division of Immunology, Mochtar Riady Institute for Nanotechnology and Medical Science Group, Pelita Harapan University, Tangerang, Indonesia.
Background: The spectrum of dengue infection ranges from asymptomatic or mild to severe disease. The pathogenic mechanisms are not fully understood. A viral infection can induce the neutrophil extracellular traps (NETs), and the excessive NETs lead to increased vascular permeability, coagulopathy, and platelet dysfunction, a hallmark of severe dengue.
View Article and Find Full Text PDFJ Hazard Mater
January 2025
College of Water Sciences, Beijing Normal University, Beijing 100875, China; Engineering Research Center of Groundwater Pollution Control and Remediation, Ministry of Education, Beijing Normal University, Beijing 100875, China.
Light nonaqueous-phase liquids (LNAPLs) are the main source of organic pollution in soil and groundwater environments. The capillary zone, with varying moisture contents, is the last barrier against the infiltration of LNAPL pollutants into groundwater and plays an important role in their migration and transformation. However, the effect and mechanism of the moisture content in the capillary zone on LNAPL pollutant migration are still unclear.
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