期刊
NEUROPROTECTIVE AGENTS
卷 1199, 期 -, 页码 125-137出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2009.05329.x
关键词
traumatic brain injury; brain edema; blood-brain barrier; blood-CSF barrier; choroid plexus; neuronal injury; cell death; Cerebrolysin; intracerebroventricular administration; sensory-motor function
资金
- Swedish Medical Research Council [2710]
- Astra-Zeneca, Molndal, Sweden
- National Institute of Health, USA [NS27601]
- Alexander von Humboldt Foundation, Germany
- Ebewe Neuro-Pharma, Austria Sweden
- The University Grants Commission, New Delhi, India
- Indian Council of Medical Research, New Delhi, India
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS027601] Funding Source: NIH RePORTER
Traumatic brain injuries (TBIs) induce profound breakdown of the blood-brain and blood-cerebrospinal fluid barriers (BCSFB), brain pathology/edema, and sensory-motor disturbances. Because neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and glial cell-derived neurotrophic factor (GDNF), are neuroprotective in models of brain and spinal cord injuries, we hypothesized that a combination of neurotrophic factors would enhance neuroprotective efficacy. In the present investigation, we examined the effects of Cerebrolysin, a mixture of different neurotrophic factors (Ebewe Neuro Pharma, Austria) on the brain pathology and functional outcome in a rat model of TBI. TBI was produced under Equithesin (3 mL/kg, i.p.) anesthesia by making a longitudinal incision into the right parietal cerebral cortex. Untreated injured rats developed profound disruption of the blood-brain barrier (BBB) to proteins, edema/cell injury, and marked sensory-motor dysfunctions on rota-rod and grid-walking tests at 5 h TBI. Intracerebroventricular administration of Cerebrolysin (10 or 30 mu L) either 5 min or 1 h after TBI significantly reduced leakage of Evans blue and radioiodine tracers across the BBB and BCSFB, and attenuated brain edema formation/neuronal damage in the cortex as well as underlying subcortical regions. Cerebrolysin-treated animals also had improved sensory-motor functions. However, administration of Cerebrolysin 2 h after TBI did not affect these parameters significantly. These observations in TBI demonstrate that early intervention with Cerebrolysin reduces BBB and BCSFB permeability changes, attenuates brain pathology and brain edema, and mitigates functional deficits. Taken together, our observations suggest that Cerebrolysin has potential therapeutic value in TBI.
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