Browsing by Subject "Blood-brain barrier"

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    Blood-brain barrier disruption following brain injury: Implications for clinical practice
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Bai, Ruojing; Ge, Xintong
    The blood-brain barrier (BBB) plays a critical role in regulating the exchange of substances between peripheral blood and the central nervous system and in maintaining the stability of the neurovascular unit in neurological diseases. To guide clinical treatment and basic research on BBB protection following brain injury, this manuscript reviews how BBB disruption develops and influences neural recovery after stroke and traumatic brain injury (TBI). By summarizing the pathological mechanisms of BBB damage, we underscore the critical role of promoting BBB repair in managing brain injury. We also emphasize the potential for personalized and precise therapeutic strategies and the need for continued research and innovation. From this, broadening insights into the mechanisms of BBB disruption and repair could pave the way for breakthroughs in the treatment of brain injury-related diseases.
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    Brain endothelial cell activation and dysfunction associate with and contribute to the development of enlarged perivascular spaces and cerebral small vessel disease
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Hayden, Melvin Ray
    Multiple injurious stimuli to the brain’s endothelium results in brain endothelial cell activation and dysfunction (BECact/dys) with upregulation of inflammatory signaling cascades and a decrease in bioavailable nitric oxide respectively. These injurious stimuli initiate a brain injury and a response to injury wound healing genetically programed cascade of events, which result in cellular remodeling of the neurovascular unit and blood-brain barrier with increased inflammation and permeability. These remodeling changes also include the perivascular spaces that become dilated to form enlarged perivascular spaces (EPVS) that may be identified noninvasively by magnetic resonance imaging. These EPVS are associated with and considered to be a biomarker for cerebral small vessel disease (SVD) and a dysfunctional glymphatic system with impaired removal of neurotoxic waste, which ultimately results in neurodegeneration with impaired cognition and dementia. The penultimate section discusses the understudied role of venous cerebral circulation in relation to EPVS, SVD, and the vascular contribution to cognitive impairment (VCID). The focus of this review will be primarily on BECact/dys that associates with and contributes to the development of EPVS, SVD, and impaired glymphatic system efflux. Importantly, BECact/dys may be a key piece of the puzzle to unlock this complicated story of EPVS and SVD. Multiple transmission electron micrographs and illustrations will be utilized to depict anatomical ultrastructure and allow for the discussion of multiple functional molecular cascades.
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    Mechanism of the protective effect of 2,3,5,4'-Tetrahydroxy stilbene-2-O-β-D-glucoside on MPTP-induced Parkinson's disease mice
    (2026) Xiaolin Dong; Qingyun Li; Yanping Li; Furong Jin; Jingting Lu; Chengda Han; Lianbing Lin; Gang Wu1; Biología Celular e Histología
    Background and purpose. Parkinson's disease (PD) is a common neurodegenerative disorder with a complex pathogenesis. 2,3,5,4'-Tetrahydroxy stilbene-2-O-β-D-glucoside (TSG) is one of the main active components of Polygonum multiflorum Thunb., which has therapeutic effects in various neurodegenerative diseases. The aim of this study was to explore the influence of TSG on the PD process. Methods. The PD mouse model was constructed via the use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The PD process was evaluated via behavioral tests, HE staining, immunohistochemistry, and immunofluorescence. The levels of related proteins and inflammatory factors were detected via western blotting and ELISA. The effect of TSG on the intestinal flora of MPTP-induced PD mice was evaluated through 16S rDNA sequencing. Results. TSG intervention can significantly alleviate motor dysfunction in PD mice, increase the number of TH-positive neurons in the substantia nigra, inhibit the accumulation of α-syn and glial cell activation, reduce the expression of the tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, iNOS, and COX2 proteins in the substantia nigra and colon, inhibit neuroinflamma-tion and intestinal inflammation, decrease the levels of LPS, LBP, TNF-α, IL-1β, and IL-6 in the serum, suppress systemic inflammation, reduce damage to the blood-brain barrier (BBB) and intestinal barrier in PD mice, and restore species diversity and abundance of the intestinal flora in PD mice to a certain extent. Conclusion. TSG can improve motor coordination ability, systemic and neuroinflammatory levels, BBB injury, intestinal barrier injury, and the intestinal flora composition of PD mice, suggesting that TSG has a protective effect on MPTP-induced PD mice.
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    Pericytes, a cell type contributing to autoimmunity and immune tolerance
    (Elsevier, 2023-06-16) Botía Sánchez, María; Molina, María Luisa; Aparicio, Pedro; Valdor Alonso, Rut; Bioquímica y Biología Molecular B e Inmunología
    Pericytes have been, since their discovery, a very hard-to-define cell because of their unknown ontogeny and the lack of specific markers. As a consequence, several attempts to characterize both its molecular pattern and its metabolism have been carried out to describe the physiological role they play. Pericytes are located in the abluminal wall of small vessels and contribute to the maintenance of capillary tone and the regulation of oxygen flow to adjacent tissues, maintaining the homeostasis of the blood-brain barrier. Furthermore, they have been described as cells with immunological properties, being able to sense and secrete proinflammatory and antiinflammatory cytokines and to activate T cells, hence controlling the immune response. Interestingly, pericytes immune function might be modulated through molecular mechanisms such as chaperone-mediated autophagy, making them to convert from immunogenic to immunosuppressive cells contributing in autoimmunity and immune tolerance. The failure of the different pericytes functions which are implicated in the brain homeostasis is related with several pathologies associated to inflammation, including type 2 diabetes, multiple sclerosis, stroke, Alzheimer's disease, and cancer. In these scenarios, pericytes have always been proved as mediators of the pathology, which indicates that this barely-known type of cell might have a wide variety of unknown roles.
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    Therapeutic potential of porphyran in mitigating ischemia-reperfusion injury in gerbil hippocampus
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Tae-Kyeong Lee; Joon Ha Park; Dae Won Kim; Choong-Hyun Lee; Moo-Ho Won; Il Jun Kang; Ji Hyeon Ahn; Biología Celular e Histología
    Cerebral ischemia-reperfusion (IR) injury is a critical pathological event that leads to extensive neuronal loss, neuroinflammation, and blood-brain barrier (BBB) dysfunction. Porphyran, a sulfated polysaccharide derived from Porphyra spp., has demonstrated anti-inflammatory and neuroprotective effects in various neurological conditions. This study aimed to evaluate the post-ischemic therapeutic potential of porphyran in a gerbil model of transient forebrain ischemia. Our findings reveal that porphyran administration (50 mg/kg orally once daily for five days) following IR significantly mitigated IR-induced cognitive decline, as evidenced by the Y-maze test, but porphyran treatment did not significantly prevent neuronal death in the CA1 subregion of the hippocampus, as revealed by Cresyl Violet (CV) and Fluoro-Jade B (FJB) staining. However, porphyran treatment after IR injury effectively attenuated the IR-induced decrease in acetylcholine (ACh) levels, suggesting potential preservation of cognitive function in surviving neurons. Furthermore, porphyran significantly mitigated microglial activation and reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), indicating its anti-inflammatory properties. Additionally, porphyran administration reduced BBB disruption, as evidenced by decreased extravasation of immuno-globulin G (IgG), suggesting a role in maintaining vascular integrity. In summary, although porphyrin administration after IR does not protect pyramidal neurons directly, it may improve cognitive function by mitigating ACh depletion, suppressing microglial activation, and reducing inflammatory cytokine levels