RESUMO
Cerebrospinal fluid (CSF) is in direct contact with the extracellular space in the central nervous system (CNS), and biological changes in the brain can be reflected in CSF. In the present article, a procedure for collection of CSF in rats is described. The technique quickly and reliably yields large quantities of CSF (50-150 microl) in rats. More importantly, blood contamination of the CSF is avoided. Furthermore, detections of ATP and interleukin (IL)-1 beta in the CSF have been carried out. ATP concentration in the CSF samples was between 8.3 and 15.8 nM, with an average of 10.5+/-0.83 nM (mean+/-SEM). The concentrations of IL-1beta were below the detection limit in the CSF in the laminectomy control rats, but it increased to 0.26+/-0.07 ng/ml at 1h after spinal cord injury. This technique offers an alternative method to surgical cannulation for the collection of CSF in rats.
Assuntos
Líquido Cefalorraquidiano , Cisterna Magna , Manejo de Espécimes/métodos , Trifosfato de Adenosina/líquido cefalorraquidiano , Animais , Sangue , Tronco Encefálico/patologia , Líquido Cefalorraquidiano/química , Ensaio de Imunoadsorção Enzimática , Interleucina-1beta/líquido cefalorraquidiano , Laminectomia , Masculino , Testes Neuropsicológicos , Ratos , Ratos Sprague-Dawley , Traumatismos da Medula Espinal/líquido cefalorraquidiano , Fatores de TempoRESUMO
In this study, we examined whether rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, is neuroprotective in focal ischemic brain injury, and whether rosiglitazone can enhance the protective action of tissue plasminogen activator (tPA), an agent used clinically for thrombolytic therapy. Rats were subjected to ischemic brain injury by embolizing preformed clots into the middle cerebral artery (MCA). Treatment with rosiglitazone reduced infarction and improved functional recovery; it also enhanced the neuroprotective action of tPA and lengthened the time window for initiating tPA treatment. Occlusion of MCA resulted in a loss of collagen type IV, a major structural protein of the microvascular basal lamina, and tPA treatment worsened this loss. Rosiglitazone treatment prevented the reduction of collagen type IV in the ischemic injured brain by inhibiting the activation of matrix metallopeptidase-9 (MMP-9). In addition, rosiglitazone treatment reduced inflammatory reactions in the ischemic injured brain. Rosiglitazone either alone or in combination with tPA is an effective agent in the reduction of ischemic brain injury. The reduction of microvascular damage and inflammation contributes to the beneficial actions of rosiglitazone.