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Objective To investigate effect of taurine on respiration chain enzyme activity of mitochondria 24 hours after severe traumatic brain injury (TBI) in rats.Methods Fifty-six SD rats were divided into sham group,TBI group,taurine treatment group,and taurine prevention group according to the random number table,with 14 rats per group.Fluid percussion brain injury models were used.Via the caudal vein,normal saline was administered to animals in sham and traumatic brain injury groups immediately after injury,while taurine (200 mg/kg)was administered to animals in taurine treatment group after injury and in taurine prevention group 4 days before injury.Brains were harvested 24 hours postinjury for assays of HE staining and electron microscopy.Mitochondrial respiratory chain complex Ⅰ-Ⅴ activities were detected.Results TBI group presented swelling neurocytes,cell loss,karyopyknosis,shortened even vanished process,and inflammation cell infiltration at the edge of necrosis in HE staining.By contrast,morphological improvement was significant in taurine treatment group but only some neurons were intact in taurine prevention group.Swelling mitochondria and broken or vanished mitochondrial crests were seen in TBI group under the electron microscope.However,normal or minor swelling mitochondria was seen in taurine treatment group and cytoplasm slightly porous and absence of mitochondrial crests were seen in taurine prevention group.Activities of complex Ⅰ,Ⅱ and Ⅴ were significant lower in TBI group (32.52±2.41,4.68 ±0.15,2.49 ±0.73) compared to those in sham group (34.03 ±0.46,5.04 ±0.29,3.20±0.68) and in taurine treatment group (33.95±0.85,5.12-±0.23,3.53 ±0.48) (P＜0.05).And complex Ⅰ in taurine prevention group was significantly enhanced as well (34.44 ± 0.36,P ＜ 0.05).Conclusion Taurine may protect the brain tissues and mitochondrial structure from impairment in TBI rats by improving mitochondrial enzymes activity and reducing secondary energy loss.
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Objective To investigate the effect of mild hypothermia on neuroprotection and prognosis prediction of rats with traumatic brain injury (TBI) by dynamically monitoring the somatosensory evoked potentials (SEP) and quantitative electroencephalogram (QEEG).Methods Forty healthy adult male SD rats were randomly divided into four groups according to random number table,ie,normal control group (with no intervention),sham operation group (fenestration only,without drilling),TBI group (fluid percussion was used to produce moderate to severe TBI),and mild hypothemia group (ice blanket was used immediately after TBI for continuous physical cooling and rectal temperature was maintained at 32-35℃ and rewarmed to 37℃ 6 hours after the initiation of cooling),with 10 rats per group.Changes of SEP and QEEG in all groups were monitored at 6,24 hours,and 7 days after TBI.Results (1) Compared with TBI group,the latency of SEP waves (P1 and N1) on the injured side in mild hypothemia group began to shorten at 24 hours(P ＜ 0.05) and were close to that in the sham operation group at 7 days.(2) Except for normal control group and sham operation group,QEEG in TBI group showed decrease of α rhythm,increase of reactivity slow waves,and decrease or disappearance of QEEG relative power spectral values at all time points.In mild hypothermia group,the reactivity slow waves were decreased with a small amount of α wave; QEEG relative power spectral values were increased at 24 hours and 7 days (especially at 24 hours),but werc still lower than those in normal control group (P ＜ 0.05).Conclusion Mild hypothermia exerts neuroprotective effect through reducing SEP latency,raising relative power spectral values of QEEG,and improving the nerve conduction and brain electrical activity of the injured side.
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Objective To study the effect of hypothermia on cerebral mitochondrial respiratory function and ultrastructure after traumatic brain injury(TBI). Methods Sprague-Dawley rats were subjected to moderate brain injury by using lateral fluid-percussion(LFP)and randomly divided into sham operation group,normothermic TBI group(rectal temperature for 36-37℃)and hypothermic TBI group(rectal temperature for 31-32℃ lasting for two hours).The ipsilateral brains were dissected and homogenized brain tissues were extracted to obtain mitochondfia by density-centrifugation and speed-centrifugation at 2,24 hours and at days 3 and 7 after TBI.The mitochondrial uhrastructure was studied by electron microscope.The indices of respiratory control rate(RCR)and P/O ratio of mitochondrial respiratory function were measured after oxygen consumption was determined with a Clark-type electrode.Results The mitochondrial uhrastructure of normothermic TBI group was damaged severely while that of hypothermic TBI group kept relatively integrated.The RCR and P/O ratio were markedly decreased two hours after TBI and reached the lowest level at the 24th hour(P＜0.01).At day 7,RCR kept at a lower level compared with sham operation group but P/O ratio recovered to normal.Change of RCR was similar in hypothermie TBI group and normothermic TBI group.However,RCR of the hypothermic TBI group was significantly higher than that of the normothermic TBI group within three days after TBI.In the meantime,P/O ratio recovered to normal three days after TBI. Conclusion Hypothermia can improve cerebral mitochondrial respiratory function and protect the mitochondrial structure after TBI.