Title |
S-Nitrosoglutathione reduces oxidative injury and promotes mechanisms of neurorepair following traumatic brain injury in rats
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Published in |
Journal of Neuroinflammation, July 2011
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DOI | 10.1186/1742-2094-8-78 |
Pubmed ID | |
Authors |
Mushfiquddin Khan, Harutoshi Sakakima, Tajinder S Dhammu, Anandakumar Shunmugavel, Yeong-Bin Im, Anne G Gilg, Avtar K Singh, Inderjit Singh |
Abstract |
Traumatic brain injury (TBI) induces primary and secondary damage in both the endothelium and the brain parenchyma, collectively termed the neurovascular unit. While neurons die quickly by necrosis, a vicious cycle of secondary injury in endothelial cells exacerbates the initial injury in the neurovascular unit following TBI. In activated endothelial cells, excessive superoxide reacts with nitric oxide (NO) to form peroxynitrite. Peroxynitrite has been implicated in blood brain barrier (BBB) leakage, altered metabolic function, and neurobehavioral impairment. S-nitrosoglutathione (GSNO), a nitrosylation-based signaling molecule, was reported not only to reduce brain levels of peroxynitrite and oxidative metabolites but also to improve neurological function in TBI, stroke, and spinal cord injury. Therefore, we investigated whether GSNO promotes the neurorepair process by reducing the levels of peroxynitrite and the degree of oxidative injury. |
X Demographics
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United States | 2 | 67% |
Unknown | 1 | 33% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 3 | 100% |
Mendeley readers
Geographical breakdown
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Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 14 | 18% |
Student > Master | 7 | 9% |
Professor > Associate Professor | 6 | 8% |
Other | 5 | 7% |
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Unknown | 16 | 21% |
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Neuroscience | 8 | 11% |
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Chemistry | 4 | 5% |
Other | 6 | 8% |
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