Protective Effect Of α-tocopherol On Neurological Function Of Traumatic Brain Injury In Rats

Objective: To investigate the protective effect of α-tocopherol on brain function and brain tissue in rats with brain injury and evaluate the therapeutic effect of α-tocopherol on rats with traumatic brain injury(TBI).Methods: One hundred and sixty adult male sprague-Dawley rats were randomly divided into sham operation group,traumatic brain injury group,conventional treatment group and conventional treatment +α-tocopherol group(α-tocopherol group),40 rats in each group.In the sham operation group,only the scalp was cut and bone window was open,and other groups were modeled by electronical controllable cortex injury(e CCl).In the conventional treatment group,anti-inflammatory treatment was conducted 7 days after TBI The α-tocopherol group was given intraperitoneal injection of α-tocopherol 200 mg / kg,Continuous injection of 7 d,sham group,TBI group were injected saline at the same time.Rats in each group were subjected to walking test of in balance beam and Morris water maze test to determine the motor function of the rats at 12 h,24 h,3 d and 7 d respectively.According to the m NSS score,the neurological function was evaluated at the corresponding time points in each group.The level of antioxidants,nitric oxide(NO),superoxide dismutase SOD),malondialdehyde(MDA),catalyze monoamine oxidative deamination reaction(MAO),in the peripheral blood of each group was determined by ELISA:.Bax,Bcl-2 expression in the brains of rats were detected by immunohistochemistry..Results:(1)In the water maze test,the time of arrival in the α-tocopherol group at 12 h,24 h,3 d and 7 d was significantly shorter than that in the TBI group and conventional treatment group(P <0.05).The treatment in the early stage of TBI is more effective in α-tocopherol group than that of the control group(P < 0.05).(2)The walking time of the balance beam in the α-tocopherol group was shorter than that in the TBI group and the conventional treatment group(P < 0.05),but the treatment of the conventional treatment group was shorter than that of the control group,the time of arrival was significantly shorter than that of TBI group at 12 h,24 h,3 d and 7 d after treatment(P < 0.05)(3)The m NSS scores of α-tocopherol group were lower than those of TBI group and conventional treatment group at 12 h,24 h,3 d and 7 d after TBI(P < 0.05),the m NSS score were lower than the TBI group(P < 0.05).(4)The degree of neurological deficit and the extent of brain damage in the α-tocopherol group were lighter than those in the TBI group and the conventional treatment group,but the degree of neurological deficit and brain tissue damage were lighter than the TBI group.(5)The edema of the brain tissue in the α-tocopherol group was lighter than that in the TBI group and conventional treatment group(P < 0.05).The edema of the brain tissue in the conventional treatment group was significantly lower than that in the TBI group(P <0.05).(6)The levels of NO and SOD in the α-tocopherol group were significantly higher than those in the TBI group and the conventional treatment group at 12 h,24 h,3 d(P < 0.05).The levels of MDA and MAO in serum in α-tocopherol were significantly lower than those in control group and TBI group(P < 0.05).The levels of NO and SOD in serum in conventional treatment group were significantly higher than those in TBI injury group at 12 h,24 h,3 d and 7 d after TBI(P < 0.05).The levels of serum MDA in 12 h,24 h,3 d,MAO was lower than that of TBI group(P <0.05).(7)The expression of Bax,in α-tocopherol group was significantly decreased while Bcl-2 was increased(P <0.05).Conclusion:(1)α-tocopherol can effectively reduce the damage of neural cells in rats with TBI,significantly improving the motor function after TBI;(2)α-tocopherol can regulate the formation of peroxide(3)α-tocopherol can reduce the brain edema and play a protective role in damaged brain tissue;(4)α-tocopherol can inhibit the expression of Bax,Bcl-2 protein And play a role in reducing the apoptosis of neural cells after TBI to protect neural function.