Bradykinin antagonist decreases early disruption of the blood–spinal cord barrier after spinal cord injury in mice
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Acknowledgements
Supported in part by the US Army Medical Research Acquisition Activity (DAMD17–00–0113), the Department of Veterans Affairs, and NIH grant HL-25284.
References (18)
- et al.
Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis
Neuron
(1994) - et al.
Murine tumor necrosis factor alpha is transported from blood to brain in the mouse
J. Neuroimmunol.
(1993) Neuroprotective signal transduction: relevance to stroke
Neurosci. Biobehav. Rev.
(1997)- et al.
BBB permeability to ebiratide and TNF in acute spinal cord injury
Exp. Neurol.
(1997) - et al.
Permeability of the blood–brain and blood–spinal cord barriers to interferons
J. Neuroimmunol.
(1997) - et al.
Tumor necrosis factor α: a neuromodulator in the CNS
Neurosci. Biobehav. Rev.
(1997) - et al.
Tumor necrosis factor facilitates regeneration of injured central nervous system axons
Brain Res.
(1991) - et al.
Tumor necrosis factors alpha and beta protect neurons against amyloid beta-peptide toxicity: evidence for involvement of a kappa B-binding factor and attenuation of peroxide and Ca2+ accumulation
Proc. Natl. Acad. Sci. USA
(1995) - et al.
Transendothelial vesicular transport of protein following compression injury to the spinal cord
Lab. Invest.
(1976)
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Neuroprotective effects of a potent bradykinin B2 receptor antagonist HOE-140 on microvascular permeability, blood flow disturbances, edema formation, cell injury and nitric oxide synthase upregulation following trauma to the spinal cord
2019, International Review of NeurobiologyCitation Excerpt :This is evident from our findings that if B2 receptors are blocked before trauma with low doses it induces neuroprotection, a feature not observed when the B2 receptors are blocked after SCI. Likewise, high doses of the B2 receptor antagonist failed to induce neuroprotection following SCI confirming the dual effects of HOE-140 (Félétou et al., 1994; Pan et al., 2001). In conclusion, our observations demonstrate that bradykinin B2 receptor antagonist HOE-140 in low doses is capable to induce neuroprotection in SCI particularly when administered 30 min before trauma.
From blood to brain through BBB and astrocytic signaling
2015, PeptidesCitation Excerpt :A dozen years ago, we noted a relatively unique pattern of upregulation of the transport system for tumor necrosis factor α (TNF) at the BBB and the associated blood–spinal cord barrier. This is seen in mouse models of spinal cord injury [44,45,48,57–59,65,67,73], traumatic brain injury [68], ischemic stroke [49], and experimental autoimmune encephalomyelitis (EAE) [46]. BBB signaling and regulatory changes are now seen in many pathophysiological conditions, including neuroAIDS [75] and inflammatory pain [9,16].
Kinin-mediated inflammation in neurodegenerative disorders
2012, Neurochemistry InternationalD-Arg-[Hyp3, IgI5, D-IgI7, Oic8]Bradykinin
2010, xPharm: The Comprehensive Pharmacology ReferenceBradykinin preconditioning induces protective effects on the spinal cord ischemic injury of rats
2008, Neuroscience Letters