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Objective The incidence of traumatic brain injury (TBI) has been on the rise year by year around the globe.According to the latest Guidelines for the Management of Severe Traumatic Brain Injury (Fourth Edition) released by the Brain Trauma Foundation (BTF),there is no sufficient evidence that related medicine can promote the repairment of neural injury in the treatment of central nerve damage.The clinical treatment of TBI is facing multiple difficulties.In recent years,brain computer interface (BCI) technology has developed rapidly and shown enormous potential in TBI repairment,especially in visual and auditory restoration,neural function recovery,and cognitive restoration.BCI provides a new approach to improve the quality of life for patients.This paper reviews the application and prospect of BCI in sense,motion,and cognitive function repairment after TBI,so as to provide new insights for the treatment of TBI nerve function.
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Objective To explore the neuroprotective effects ofβ-aescinate on brain edema in rats of traumatic brain injury (TBI). Methods A total of 78 male SD (Sprague Dawley) rats were randomly divided into three groups: sham-operation group (Sham), traumatic brain injury group (TBI) andβ-aescinate group, with 26 rats in each group. Rats of Sham group were anesthetized and surgically prepared only, but were not induced by cortical contusion. Electronic brain cortical damage impactor (eCCI) was used for establishing TBI model in TBI group and β-aescinate group after opening the bone window. TBI group was only established TBI model, but no intervention. After establishment of TBI model in β-aescinate group, β-aescinate (5 mg/kg body weight) was intraperitoneally injected, once every 24 hours. The modified neurological severity scores (mNSS) was used for evaluating changes of neurological function. After 48 hours, SD rats were sacrificed for hematoxylin and eosin (H&E) staining (n=6). Additionally, water content of the brain tissue was evaluated using the wet-to-dry weight ratio (n=10). Evans blue assay was performed to investigate the blood-brain barrier (BBB) permeability (n=4). The expression of aquaporin 4 (AQP4) was measured by Western blot assay (n=6). Results Compared with the Sham group, neurologic deficit, increased brain water content and the expression of AQP4 were found in TBI group (all P<0.05). Moreover, BBB permeability was destroyed. However, β-aescinate can improve the neurological function, reduce the brain water content and significantly decrease the expression of AQP4 in TBI rats. The BBB permeability was significantly improved in treatment group (all P<0.05). Conclusion These findings suggest that β-aescinate can reduce cerebral edema and improve neurological outcome in SD rats after TBI. This neuroprotection may be related with the down-regulation of AQP4 protein.
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Objective To investigate the inhibitory effects of N-acetylcysteine (NAC) on inflammatory factors after acute spinal cord injury, and the mechanisms thereof. Methods A total of 54 clean and healthy adult female SD rats were divided into three groups according to the principle of randomization:simple laminectomy group (Sham group), spinal cord injury group (SCI group) and N-acetylcysteine group (NAC group), with 18 rats in each group. The Sham group was treated with T9-10 laminectomy only without spinal cord injury. Aneurysm clamp was used to establish rat model of T9-10 spinal cord injury in SCI group and NAC group. At the time of 15 min and 12 h after injury, the rats of NAC group were injected N-acetylcysteine intraperitoneally (150 mg/kg). At the time of 24 h post modeling, 12 rats were sacrificed in each group for observing the severity of tissue injury by using hematoxylin-eosin (HE) staining (6 rats), and detecting the contents of inflammation factors including tumor necrosis factor (TNF)- α and interleukin (IL)- 6 by using enzyme- linked immunosorbent assay (ELISA) (6 rats). The remaining 6 rats in each group were raised for 8 weeks. During the first week, the ones in NAC group were injected NAC twice a day at 12 h intervals for 7 d. Additionally, the neurological function evaluation was performed at week 1, week 2, week 4, week 6 and week 8 after injury in rats by using the spinal cord injury motor function score (BBB) and the inclined plate test. Results The results of HE staining showed that the spinal cord was intact without hemorrhage and inflammatory cell infiltration in Sham group. The morphology and inflammatory status were significantly worse in SCI group than those in NAC group and Sham group. The results of ELISA showed that the expressions of TNF-αand IL-6 were significantly higher in SCI group and NAC group than those in Sham group (P<0.05), while the expression levels of TNF-αand IL-6 were significantly lower in NAC group than those of SCI group (P<0.05). The BBB scores and inclined plate test showed that both were significantly lower in SCI group and NAC group than those of Sham group (P<0.05), and the results were better in NAC group than those of SCI group. Conclusion NAC may promote the recovery of neurological function in rats by reducing the local inflammatory response through diminishing the contents of TNF-αand IL-6 in spinal cord.