RESUMEN
To date, the therapeutic methods for ischemic and hemorrhagic stroke are still limited. The lack of oxygen supply is critical for brain injury following stroke. Hyperbaric oxygen (HBO), an approach through a process in which patients breathe in 100% pure oxygen at over 101 kPa, has been shown to facilitate oxygen delivery and increase oxygen supply. Hence, HBO possesses the potentials to produce beneficial effects on stroke. Actually, accumulated basic and clinical evidences have demonstrated that HBO therapy and preconditioning could induce neuroprotective functions via different mechanisms. Nevertheless, the lack of clinical translational study limits the application of HBO. More translational studies and clinical trials are needed in the future to develop effective HBO protocols.
RESUMEN
Neurosurgical operations may result in surgical injury which would lead to postoperative neurological deficits. Hyperbaric oxygen preconditioning (HBO-PC) may be beneficial for such people. However, the exact mechanism underlying HBO-PC is not well known yet. The aim of this study is to explore the role of osteopontin (OPN) in HBO-PC-induced neuroprotection. The study consisted of two experiments. In experiment 1, Sprague Dawley (SD) rats were divided into four groups: sham group, HBO-PC sham group, stroke group, and HBO-PC group (HBO-PC + stroke). The animals in the second experiment were randomly assigned to one of two groups: OPN small interfering (siRNA) group (HBO-PC + stroke + OPN siRNA) and control siRNA group (HBO-PC + stroke + negative control siRNA). Neurological outcome in HBO-PC group was better than that of stroke group. After OPN siRNA was administered, neurological function aggravated compared with control siRNA group. Brain morphology and structure seen by light microscopy was diminished in stroke group and OPN siRNA group, while fewer pathological injuries occurred in HBO-PC and control siRNA group. The infarct volume in HBO-PC group was the lowest, followed by OPN siRNA group and stroke group, respectively. Preconditioning with HBO promoted expression of OPN, which reduced the expression of interleukin (IL)-1ß/nuclear factor-κ-gene binding (NFκB) and augmented protein kinase B (Akt). OPN siRNA reversed these changes. OPN plays an important role in the neuroprotection elicited by HBO-PC. Pretreatment with HBO may be beneficial for people going to undertake brain surgery.
Asunto(s)
Isquemia Encefálica/metabolismo , Oxigenoterapia Hiperbárica , Precondicionamiento Isquémico , Neuroprotección , Osteopontina/metabolismo , Accidente Cerebrovascular/complicaciones , Accidente Cerebrovascular/metabolismo , Animales , Encéfalo/metabolismo , Encéfalo/patología , Isquemia Encefálica/complicaciones , Isquemia Encefálica/patología , Regulación hacia Abajo , Interleucina-1beta/metabolismo , Masculino , FN-kappa B/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Interferente Pequeño/metabolismo , Ratas Sprague-Dawley , Accidente Cerebrovascular/patología , Regulación hacia ArribaRESUMEN
BACKGROUND: It is a common belief that neurosurgical interventions can cause inevitable damage resulting from the procedure itself in surgery especially for intramedullary spinal cord tumors. The present study was designed to examine if hyperbaric oxygen preconditioning (HBO-PC) was neuroprotective against surgical injuries using a rat model of spinal cord injury (SCI). METHODS: Sprague-Dawley rats were randomly divided into three groups: HBO-PC group, hypobaric hypoxic preconditioning (HH-PC) control group, and normobaric control group. All groups were subjected to SCI by weight drop device. Rats from each group were examined for neurological behavior and electrophysiological function. Tissue sections were analyzed by using immunohistochemistry, TdT-mediated dUTP-biotin nick end labeling, and axonal tract tracing. RESULTS: Significant neurological deficits were observed after SCI and HBO-PC and HH-PC improved neurological deficits 1 week post-injury. The latencies of motor-evoked potential and somatosensory-evoked potential were significantly delayed after SCI, which was attenuated by HBO-PC and HH-PC. Compared with normobaric control group, pretreatment with HBO and hypobaric hypoxia significantly reduced the number of TdT-mediated dUTP-biotin nick end labeling-positive cells, and increased nestin-positive cells. HBO-PC and HH-PC enhanced axonal growth after SCI. CONCLUSIONS: In conclusion, preconditioning with HBO and hypobaric hypoxia can facilitate functional recovery and suppress cell apoptosis after SCI and may prove to be a useful preventive strategy to neurosurgical SCI.