Research reportInhibition of nitric oxide synthase attenuates blood-brain barrier disruption during experimental meningitis
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Breaking barriers: Neurodegenerative repercussions of radiotherapy induced damage on the blood-brain and blood-tumor barrier
2022, Free Radical Biology and MedicineToxocara-induced neural larva migrans (neurotoxocarosis) in rodent model hosts
2020, Advances in ParasitologyCitation Excerpt :Beside microglia activation, elevated glial fibrillary acidic protein (GFAP)-expression has been detected by immunohistochemistry, providing evidence for astrocytic activation and reactive astrogliosis in the cerebral parenchyma (Eid et al., 2015; Liao et al., 2008; Othman et al., 2010). Furthermore, T. canis-infection causes an elevated expression of inducible nitric oxide synthase (iNOS) in glial cells, which can have detrimental effects on the brain if produced in excess (Boje, 1996; Gargili et al., 2004; Liao et al., 2008; Othman et al., 2010). Neuroinflammatory processes are initiated by potent pro-inflammatory cytokines, e.g., TNF-α, interferon (IFN)-γ and IL-6, but excessive or inappropriate neuroinflammatory reactions may be detrimental for cerebral tissues.
Acute Meningitis
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesCritical role of TRPP2 and TRPC1 channels in stretch-induced injury of blood-brain barrier endothelial cells
2012, Brain ResearchCitation Excerpt :Our current studies demonstrate that stretch-induced activation of TRPC1 and TRPP2 lead to both a rapid activation of calcium influx that, in turn, leads to activation of eNOS and the generation of NO. Both elevated cytosolic calcium levels and NO levels likely contribute to altered endothelial functions under these conditions and loss of integrity of the endothelial barrier. Indeed accumulating evidence points to an NO-mediated modulation of barrier permeability in endothelial cells (Boje, 1996; Boueiz and Hassoun, 2009), including mechanisms involving actin-cytoskeleton modifications (Shen et al., 2010; Yuan et al., 1997). Further, several TBI studies have reported a rise of NO levels shortly after injury which may contribute to barrier breakdown (Rao et al., 1998; Wada et al., 1998).
Contribution of nitric oxide synthase (NOS) in blood-brain barrier disruption during acute focal cerebral ischemia in normal rat
2012, PathophysiologyCitation Excerpt :Although, disruption of BBB integrity due to ischemic/reperfusion (I/R) injury during stroke is well documented [3,12], data about the involvement of NO are conflicting. Some reports have demonstrated that the inhibition of nitric oxide synthase (NOS) activity by l-NAME diminished acute ischemic brain damage by reducing BBB disruption [12,13]. Whereas, others have revealed that the administrations of l-arginine, NO substrate, reduced ischemic brain damages by endorsing NO-dependent vasodilatation pathway and increasing regional cerebral blood flow (rCBF) [14–16], whereas others believe it augmented ischemic neural damages by increasing tissue NO production [17].