TY  - JOUR
PY  - 2013//
TI  - Blast induces oxidative stress, inflammation, neuronal loss and subsequent short-term memory impairment in rats
JO  - Neuroscience
A1  - Cho, Hyung Joon
A1  - Sajja, Venkata Siva Sai Sujith
A1  - Vandevord, Pamela J.
A1  - Lee, Yong Woo
SP  - 9
EP  - 20
VL  - 253
IS  - 
N2  - Molecular and cellular mechanisms of brain injury after exposure to blast overpressure (BOP) are not clearly known. The present study hypothesizes that pro-oxidative and pro-inflammatory pathways in brain may be responsible for neuronal loss and behavioral deficits following BOP exposure. Male Sprague Dawley rats were anesthetized and exposed to calibrated BOP of 129.23 ± 3.01 kPa while controls received only anesthesia. In situ dihydroethidium (DHE) fluorescence staining revealed that BOP significantly increased production of reactive oxygen species (ROS) in the brain. In addition, real-time reverse transcriptase-polymerase chain reaction (RT-PCR), immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA) demonstrated a significant up-regulation of mRNA and protein expressions of pro-inflammatory mediators, such as interferon-γ (IFN-γ) and monocyte chemoattractant protein-1 (MCP-1), in brains collected from BOP-exposed animals compared with the controls. Furthermore, immunoreactivity of neuronal nuclei (NeuN) in brains indicated that fewer neurons were present following BOP exposure. Moreover, novel object recognition (NOR) paradigm showed a significant impairment in the short-term memory at 2 weeks following BOP exposure. These results suggest that pro-oxidative and pro-inflammatory environments in brain could play a potential role in BOP-induced neuronal loss and behavioral deficits. It may provide a foundation for defining a molecular and cellular basis of the pathophysiology of blast-induced neurotrauma (BINT). It will also contribute to the development of new therapeutic approaches selectively targeting these pathways, which have great potential in diagnosis and therapy for BINT.<p />  <p>Language: en</p>
LA  - en
SN  - 0306-4522
UR  - http://dx.doi.org/10.1016/j.neuroscience.2013.08.037
ID  - ref1
ER  -