Williams Anthony J, Ling Geoff, McCabe R Tyler, Tortella Frank C
Department of Neuropharmacology and Molecular Biology, Division of Neurosciences, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA.
Neuroreport. 2002 May 7;13(6):821-4. doi: 10.1097/00001756-200205070-00017.
The NMDA antagonist CGX-1007 (Conantokin-G) has previously been shown to possess potent neuroprotective properties when administered intracranially following experimental ischemic brain injury. Using the same model of middle cerebral artery occlusion (MCAo) in rats we now report the neuroprotective effects of CGX-1007 when delivered intrathecally (i.t.). When given 4 h post-occlusion, a reduction in brain infarction was measured along with significant neurological recovery. Furthermore, we describe an i.t. neuroprotective therapeutic window lasting > or = 8 h from the start of the injury. Critically, this is the first comprehensive report of a neuroprotective agent that can be administered i.t. to ameliorate experimental brain injury and potentially provide an excellent therapeutic window as a neuroprotection treatment.
NMDA拮抗剂CGX-1007(芋螺毒素G)先前已被证明,在实验性缺血性脑损伤后经颅内给药时具有强大的神经保护特性。我们利用相同的大鼠大脑中动脉闭塞(MCAo)模型,现在报告经鞘内(i.t.)给药时CGX-1007的神经保护作用。在闭塞后4小时给药,可测量到脑梗死面积减小,同时神经功能有显著恢复。此外,我们描述了一个从损伤开始起持续≥8小时的鞘内神经保护治疗窗。至关重要的是,这是关于一种可经鞘内给药以改善实验性脑损伤并可能作为神经保护治疗提供极佳治疗窗的神经保护剂的首份全面报告。