Daily Administration of Ibuprofen Modifies Neuroinflammation Gene Expression, but not Neuroplasticity Gene Expression in Traumatic Brain Injured Rats
Each year there are at least 1.4 million civilian traumatic brain injury (TBI) incidents, with most as a result of a moderate level of injury and being treated in the emergency department (Langlois and Sattin 2005). The post-traumatic morbidity is likely to result from secondary molecular, biochemical and cellular events that cause additional neuronal, glial and vascular injuries across multiple brain areas (Thompson, Gibson et al., 2006; Farkas and Povlishock 2007).
One of the primary histopathological consequencesassociated with TBI is microglial activation and ensuing neuroinflammation(Csuka, Hans et al. 2000). Inflammation in neurodegenerative conditions can be both detrimental and beneficial(Gensel, Nakamura et al. 2009). Inflammation can clear dead or dying tissue. On the other hand, previous studies in spinal cord injury and Alzheimer diseases have shown that microglia activation, especially the alternative activation of microglia, can be one factor that promotes neuroplasticity and potentially affect the recovery of the patient (Donnelly and Popovich, 2008; Popovich and Longbrake, 2008; Colton, 2009; Colton and Wilcock, 2009; Gensel, Nakamura et al., 2009; Kigerl, Gensel et al., 2009). We hypothesize that the
primary mechanical forces of TBI initiate microglia activation, and therefore anti-inflammatory treatments would reduce microglia activation, helping to control post-traumatic neuroplasticity. Here, we examine the post-traumatic microglia activation states: classical activation associated with neurotoxicity, alternative activation associated with recovery, and acquired deactivation associated with anti-inflammatory response (Colton and Wilcock, 2009; Gensel, Nakamura et al., 2009). Also, we examine the ability of the anti-inflammatory ibuprofen to modulate microglial activation and neuroplasticity gene expression using real-time PCR.