tailieunhanh - Báo cáo y học: " Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats. | Lai et al. Journal of Biomedical Science 2011 18 69 http content 18 1 69 The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats Pdi Lhi in I n11 2 Von Tn I 11 I n m cn1 3 6 Thin chũn A I4 Tiin n- I mn I n I2 Pnn II inn A nnci2 wl Tool I I Thill1 6 Pei dun Lal Ten la Huang Cilla den wu Clung Jung Lal Pen Jung wang and leu H Chiu Abstract Background Perinatal brain injury is the leading cause of subsequent neurological disability In both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy HIE . Glutamate transporter GLT1 expressed mainly in mature astrocytes is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds such as ceftriaxone that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Methods We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8 oxygen for 2 hrs on postnatal day 7 P7 rats. Neonatal rats were administered three dosages of an antibiotic ceftriaxone 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Results Pre-treatment with 200 mg kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus restored myelination in the external capsule of P14 rats and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Conclusion These results .