@article {Wang:2015:1791-2997:2149,
title = "Neuroprotective effectsof brilliant blue G on the brain following traumatic brain injury in rats",
journal = "Molecular Medicine Reports",
parent_itemid = "infobike://sp/mmr",
publishercode ="sp",
year = "2015",
volume = "12",
number = "2",
publication date ="2015-08-01T00:00:00",
pages = "2149-2154",
itemtype = "ARTICLE",
issn = "1791-2997",
eissn = "1791-3004",
url = "https://www.ingentaconnect.com/content/sp/mmr/2015/00000012/00000002/art00075",
doi = "doi:10.3892/mmr.2015.3607",
author = "Wang and Cui and Cui and Sun and Cui and Zhang and Zhu and Li and Tian and Gao",
abstract = "The P2X7inhibitor,brilliant blue G (BBG), has been reported as a neuroprotective drug against a variety of disorders, including neuropathic pain and brain ischemia. Currently, no studies have examined the potential for BBG to provide neuroprotection in animal models of TBI.
The aim of the present study was to investigate the neuroprotective effect of BBG on TBI and to determine the underlying mechanisms. The rats were subjected to a diffuse cortical impact injury caused by a modified weightdrop device, and then divided randomly into three groups: the shamoperated,
BBG treatment and vehicle groups. In the BBG treatment group, 50mg/kg brilliant blue G (BBG; 100% pure), a highly specific and clinically useful P2X7 antagonist, was administered via the tail vein 15 min prior to or up to 8h following TBI. The colocalization of NeuN and protein
kinase C (PKC) was followed with immunofluorescent staining. The expression of P2X7, PKC and inflammatory cytokines was identified by western blot analysis. Wetdry weight method was used to evaluate brain edema, and motor function outcome was examined using the neurological
severity score. The present study demonstrated that the administration of BBG attenuated TBIinduced cerebral edema and the associated motor deficits. Following trauma, BBG treatment significantly reduced the levels of PKC and interleukin1 in the cortex. The results provide invivo
evidence that BBG exerted neuroprotective effects by attenuating brain edema and improving neurological functions via reducing PKC and interleukin-1 levels following TBI.",
}