Résumé
Objective To investigate the changes of the level of oxidative stress and cell apoptosis of secondary brain injury after traumatic brain injury,and the influence of brain-derived neutrophic factor on these parameters in rats,as well as its potential mechanisms.Methods A total 84 adult and healthy male rats was divided randomly into 2 groups:control (n =42) and traumatic brain injury (TBI) groups (n =42).The brain-derived neurotrophic factor (BDNF) group was induced using improved Feeney method and was received abdominal injections of BDNF (0.5 μg/μl) immediately after injury,the control group were received abdominal injections with the same dose sodium chloride injection immediately after injury and repeat one time everyday until the rats was killed.Each group was divided into seven subgroups by sacrificed time after injury,those are 1 h,3 h,6 h,12 h,24 h,3 d,and7 d,each subgroup got6 rats.Each subgroup was randomly selected three rats after being killed.The water content,superoxide dismutase (SOD),malonic aldehyde (MDA),and glutathione (GSH) of rats were measured contusion peri tissues brain tissue.Specimens were taken from left three rats of subgroup,which was part of the brain tissue.The expression of NF-κB p65,around the brain tissue with immunohistochemical methods were detected.TdT-mediated dUTP nick-end labeling (TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results NF-κB p65 was expressed obviously around the lesion in 1h group,and strongly expressed in TBI-3 h-12 h,and reached a peak in 24 h after the injury,while NF-κB p65 expression reduced in TBI-3 d-7 d,and still in high expression.NF-κB p65 expression strongly correlated with the degree of cerebral edema (r =0.651,P ＜0.05).For two groups,NF-κB p65 expression strongly correlated with the level of MDA (r1 =0.947,P ＜0.01;r2 =0.961,P ＜0.01).Conclusions Changes of NF-κB protein expression after brain injury were involved in a series of pathological processes of secondary brain injury,such as oxidative stress,and apoptosis,brain-derived neutrophic factor is probably through inhibit oxidative stress levels,control apoptosis,prevent the development of vasogenic cerebral edema,and reduce or mitigate secondary brain injury.
Résumé
Objective To investigate the changes of NF-κB p65, IL-6 and cell apoptosis in sec-ondary brain injury after traumatic brain injury and the influence of fenofibrate on these parameters in rats. Methods Ninety-eight male Sprague-Dawley ( SD) rats were randomly divided into two groups:fenofibrate group ( n =49) and control group ( n =49) .The fenofibrate group was induced with the improved Feeney method and received intragastrica of lipanthyl 60 mg/(kg? d) immediately after injury.The control group were received intragastrica of sodium chloride injection 2 ml/( kg? d) immediately after injury and twice everyday until rats were killed.Each group was divided into seven subgroups by sacrificed time after injury, those were 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, and 7 d, and each subgroup got 7 rats.Each subgroup was ran-domly selected three rats after being killed to detect expressions of NF-κB p65 and IL-6 of rat contusion peri tissues brain tissues with immunohistochemical method.While using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling ( TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results The expressions of NF-κB p65 and the IL-6 in each fenofibrate group were significantly decreased relative to the control group ( P <0.05),and a significant positive correlation between both pa-rameters in two groups ( P <0.01) .At the same time, the number of apoptotic cells was decreased ( P <0.05).Conclusions Fenofibrate was probably through the route of relieving inflammation response to re-duce the change of secondary brain injury after traumatic brain injury and decrease neural cell apoptosis, and then provide protection of neurocytes.
Résumé
[Objective]To study the risk factors of neurosurgical postoperative intracranial infection.[Methods]Analyse 30 cases of intracranial infection after the neurosurgery operation from 2003 to 2008 in our department.[Results]The intracranial infections after craniocerebral operation is related to the operation duration,cerebrospinal fluid leakage,external ventricular drainage,laying the drainage-tube,open craniocerebral injury.[Conclusion]To shorten the operation time as long as possible,tighten dural closure to prevent leakage of cerebrospinal fluid,with strict control of the indwelling time, reduce the number of drainage-tube and shorten indwelling time after neurosurgery operation as possible as we can,can reduce the possibility of intracranial infection after neurosurgery operation.