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Objective@#To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism.@*Methods@#A total of 96 SD rats were randomly divided into sham operation group, sham operation+ propofol group, TBI group and TBI + propofol group, with 24 rats in each group. The TBI model was prepared by modified Feeney method. The sham operation+ propofol group and the TBI+ propofol group were given 50 mg/kg of propofol once daily. The sham operation group and the TBI group were injected with the same amount of normal saline. Modified neurobehavioral functional scores (mNSS) were evaluated at 1, 3, 7 and 14 days after injury; dry-wet specific gravity method was used to detect brain water content in injured area; TUNEL staining was used to detect neuronal apoptosis; chemiluminescence was used to detect activity of Oxygen cluster (ROS) content; Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1), enhancer binding protein homolog protein (CHOP), heme oxygenase 1 (HO-1), quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein.@*Results@#Compared with the sham operation group and the sham operation + propofol group, the mNSS, brain tissue water content, apoptosis number and ROS increased at 1, 3, 7 and 14 days after TBI in the TBI group and TBI + propofol group (P<0.05). Compared with TBI group, mNSS in TBI+ propofol group decreased significantly [(9.3±1.4)points ∶(10.9±1.2)points] 7 days after injury (P<0.05); the brain tissue water content decreased significantly [(81.0±0.8)%∶(82.1±0.8)%] 3 days after injury (P<0.05); the number of apoptotic cells decreased significantly 7 days after injury[(14.1±1.4)%∶(15.6±1.6)%], with the most significant decrease at 14 days after injury [( 10.4±1.5)%∶(13.2±1.4)% (P<0.05); and ROS decreased significantly 7 days after injury [(61.5±4.0)RFU∶(77.3±5.5)RFU](P<0.05). Compared with the sham operation group and the sham operation+ propofol group, the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI+ propofol group (P<0.05); the expressions of HO-1, NQO1 and Nrf2 in the TBI group were significantly decreased (P<0.05); the expressions of HO-1 and NQO1 in TBI+ propofol group were increased (P<0.05) while the expression of Nrf2 were decreased slightly (P<0.05). Compared with the TBI group, the expressions of IRE-1 and CHOP in TBI+ propofol group were decreased (P<0.05), while the expressions of HO-1, NQO1 and Nrf2 were significantly increased (P<0.05).@*Conclusion@#After TBI in rats, propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway, reduce brain edema, and inhibit neuronal apoptosis, thus playing a neuro-protective role.
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Objective To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism.Methods A total of 96 SD rats were randomly divided into sham operation group,sham operation + propofol group,TBI group and TBI +propofol group,with 24 rats in each group.The TBI model was prepared by modified Feeney method.The sham operation + propofol group and the TBI + propofol group were given 50 mg/kg of propofol once daily.The sham operation group and the TBI group were injected with the same amount of normal saline.Modified neurobehavioral functional scores (mNSS) were evaluated at 1,3,7 and 14 days after injury;dry-wet specific gravity method was used to detect brain water content in injured area;TUNEL staining was used to detect neuronal apoptosis;chemiluminescence was used to detect activity of Oxygen cluster (ROS) content;Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1),enhancer binding protein homolog protein (CHOP),heme oxygenase 1 (HO-1,quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein.Results Compared with the sham operation group and the sham operation + propofol group,the mNSS,brain tissue water content,apoptosis number and ROS increased at 1,3,7 and 14 days after TBI in the TBI group and TBI + propofol group (P ＜ 0.05).Compared with TBI group,mNSS in TBI + propofol group decreased significantly [(9.3 ± 1.4) points ∶ (10.9 ± 1.2) points] 7 days after injury (P ＜ 0.05);the brain tissue water content decreased significantly [(81.0 ± 0.8) ％ ∶ (82.1 ± 0.8) ％] 3 days after injury (P ＜ 0.05);the number of apoptotic cells decreased significantly 7 days after injury [(14.1 ± 1.4) ％ ∶ (15.6 ± 1.6) ％],with the most significant decrease at 14 days after injury [(10.4 ± 1.5) ％ ∶ (13.2 ± 1.4) ％ (P ＜ 0.05);and ROS decreased significantly 7 days after injury [(61.5 ± 4.0) RFU∶ (77.3 ± 5.5) RFU] (P ＜ 0.05).Compared with the sham operation group and the sham operation + propofol group,the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI + propofolgroup (P ＜ 0.05);the expressions of HO-1,NQO1 and Nrf2 in the TBI group were significantly decreased (P ＜0.05);the expressions of HO-1 and NQO1 in TBI + propofol group were increased (P ＜0.05) while the expression of Nrf2 were decreased slightly (P ＜ 0.05).Compared with the TBI group,the expressions of IRE-1 and CHOP in TBI + propofol group were decreased (P ＜ 0.05),while the expressions of HO-1,NQO1 and Nrf2 were significantly increased (P ＜ 0.05).Conclusion After TBI in rats,propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway,reduce brain edema,and inhibit neuronal apoptosis,thus playing a neuro-protective role.
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Objective To investigate the effects and mechanisms of valproic acid on brain edema,neurobehavioral outcome and inflammatory response after traumatic brain injury (TBI) in rats.Methods TBI animal models were established using Feeney's method.Fifty-four SD male rats,weighting 220-250 g,were randomly divided into 3 groups (n =18):sham operation group (group sham),traumatic brain injury group (group TBI) and valproic acid treatment group (group TBI + VPA).Experimental rats were treated with valproic acid (300 mg/kg,twice daily) by intraperitoneal injection.Rat behavioral outcomes were measured by modified neurologic severity score (mNSS) tests at day 1,3,and 7 after TBI.Brain water content was measured with wet-dry weight method.The blood cells infiltration into cerebral cortex were tested with immunohistochemistry staining against ED-1 for macrophage.Inflammatory cytokines (INF-γ,tumor necrosis factor-α,interleukin-6) were measured by Western blotting.The statistical analysis were performed by ANOVA and chi-square tests using the statistical software program SPSS 13.0.Results Compared with the Sham group,the levels of brain edema,mNSS and macrophage cell infiltration were significantly increased after TBI (all P =0.00).The expressions of inflammatory cytokines were also increased significantly (all P =0.00).Compared with the TBI group,TBI + VAP group had significantly lower brain water content[3day:(80.12 ±0.59)％ vs.(82.14 ±0.67)％,P=0.04;7day:(74.74 ±0.72)％ vs.(77.93 ±0.48)％,P=0.01],and mNSS scores [3 day:(10.53 ±0.32) vs.(11.74 ±0.48),P =0.02;7 day:(7.97 ± 0.32) vs.(10.73 ± 0.42),P =0.01].VPA suppressed macrophage cell infiltration into cerebral cortex [(36.44 ± 0.72) ％ vs.(25.93 ± 0.48) ％ P =0.00].Meanwhile,VPA inhibited the expressions of inflammatory cytokines (INF-γ,TNF-α,IL-6) (P ＜ 0.05).Conclusions Treatment with VPA markedly reduced brain edema and improved neurological outcomes after TBI,possibly mediated by inhibited TBI-induced cerebral inflammatory responses and macrophage cell infiltrating into cerebral cortex.
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As a transmembrane protein, β-amyloid precursor protein(β-APP) distributes extensively in the central nervous system, has the effect of neurotrophic, and neuroprotective, promote neurite growth and synaptogenesis, β-amyloid(Aβ) is the digestion products of its precursor-APP in the pathological conditions, and it is the main component of senile plaques-the main pathological changes of Alzheimer' s disease (AD), its toxic effects can also induce neuronal apoptosis, The expression of the two proteins after brain injuried has a close relationship with the injury, cognitive dysfunction, Alzheimer' s disease and the pathophysiological changes of central nervous system. To explore its expression in the brain after traumatic brain injury can determine the degree of injury, assess the prognosis and open up new avenues for the treatment of traumatic brain injury.
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Objective To investigate the safety of autologous blood component transfusion during cesarean section in patients with Rh (D)-negative blood group.Methods Thirty ASA Ⅰ or Ⅱ patients of Rh (D)-negative blood group, aged 20-35 yr, weighing 50-80 kg, undergoing elective cesarean section, were enrolled in this study.After lactated Ringer' s solution 7 ml/kg was infused, blood was obtained from radial artery at a rate of 60-80ml/min, and blood volume was maintained by simultaneous infusion of 6% hydroxyethyl starch 130/0.4 at the same rate. The collected blood was subjected to two cycles of autologous blood component separation. Blood collecting during each cycle was stopped 15 s after red blood cells were separated. The autologous blood was infused when the blood loss≥20% of blood volume. The autologous blood was infused after suture of the uterus when the blood loss < 20% of blood volume. The parameters of maternal vital signs and fetal heart rate were monitored. Hypotension and tachycardia were recorded during autologous blood collecting. SpO2 was monitored routinely. Venous blood samples were taken before blood collecting (baseline), at the end of blood collecting, before autologous blood transfusion, 24 h after operation for determination of Hb, Hct, Plt, PT, APTT, INR and Fib. Umbilical arterial blood samples were obtained after delivery for blood gas analysis. Apgar score was recorded at 1 and 5 min after birth. Blood loss and allogeneic blood transfusion were also recorded. Results No hypotension and tachycardia occurred during the process of blood collecting and the fetal heart rate was within the normal range. Compared with the baseline value, there were no significant differences in SpO2 , Hb, Hct, Plt, PT, APTT, INR and FIB value at the other time points. The pH value and concentrations of base excess and lactate were within the normal range.The Apgar score was (9.0 ±0.8) and (9.2 ± 0.8) at 1 and 5 min after birth respectively. The blood loss during operation was (405 ± 28) ml and no patients received homologous blood transfusion. Conclusion The safety of autologous blood component transfusion is good during cesarean section in Rh (D)-negative blood group patients.
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Objective To investigate the possible pathogenesis of the cognitive function in unilateral frontal bottom laceration by follow-up study in patients after one month of the onset. Methods MMSE, Loewenstein Occupational Therapy Cognitive Assessment (LOTCA), Montreal Cognitive Assessment (MoCA), Wisconsin Card Sorting Test (WCST) scales were used to evaluate neurocognitie function in 42 patients after one month of onset of unilateral frontal bottom laceration and 45 normal controls. The wave amplitude and the latency of the endogenous composition N2, P3 of P300 were measured at the cognitive potential instrument. Level of AChE was determined by ELISA and active AChE was analyzed by the ration analyses. Stepwise multivariate regression analyzed the correlation of the overall cognitive function and the lever and active of AChE. Results The cognitive test scores in patients were significantly worse than those in normal controls. The ability of recite sentences, fluency of words, reading, understanding language,cognitive transfering decreases in the left frontal bottom laceration patients (Group A, 23 cases), while the ability of attention, action, organization, graphics depicting, abstract epitoming, logical thinking were all seriously impaired in the patients with right frontal bottom laceration (Group B, 19 cases). The latency of the endogenous composition N2, P3 in patients ( Group A: (322. 4 ± 17.0), (410. 1 ± 19.9) ms; Group B:( 308.4 ± 15.6), (385.5 ± 17.4) ms) is more lengthen ( F = 4. 084, P = 0. 018; F = 3.467, P = 0. 038 )than the normal controls ( (268.6 ± 14. 7 ), ( 369. 2 ± 15. 4 ) ms) and the wave amplitude is lower ( F =2. 986 ,P =0. 047 ;F =3. 313 ,P =0. 041 ). The latency of N2 ,P3 in Group A of is more lengthen than Group B, while the wave amplitude is higher. The difference of the active of AChE in patients and control groups had no statistical significance, however, the level of AChE in two groups had statistical significance. The comparison of the active and the total AChE in patients has also not statistical significance. The correlation of the overall cognitive function has the linear regression with the parts of the brain and the level of AChE ( rY1.2 = 0. 584, P = 0. 039; rY2.1 = 0. 726, P = 0. 017 ). The standardized regression coefficients showed the level of AChE has the biggest influence to the overall cognitive function ( |Beta| =0. 3601, rY2.1 =0. 726).Conclusions AChE may be one of the important factors in the cognitive function after frontal bottom laceration. The specific damages of cognitive function in unilateral frontal bottom laceration patients closely relate with the lesion locations in the injured frontal bottom laceration.
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70%)in 3 cases with MDS and in 4 cases with GDC,Partial(