BACKGROUND： Mechanical injury can cause the changes of polygene expression spectrum in rat cerebral cortical nerve cells, and then result in the changes of intracellular protein expression. At present, dielectrophore...BACKGROUND： Mechanical injury can cause the changes of polygene expression spectrum in rat cerebral cortical nerve cells, and then result in the changes of intracellular protein expression. At present, dielectrophoresis is combined with mass spectrum technique to detect the expression of different proteins in rat cortex after brain injury, but the protein chip technique requires further investigation. OBJECTIVE： To analyze the differences of protein expression spectrum in rat cerebral cortex before and after closed traumatic brain injury using WCX-2 protein chip technique. DESIGN： A randomized controlled animal experiment. SETTING： Training Division of the Medical College of Chinese People＇s Armed Police Force. MATERIALS： Seventy-two male SD rats of clean degree, 350 - 450 g, were provided by the Experimental Animal Center, Academy of Military Medical Sciences of Chinese PLA. Urea, trifluoroacetic acid, CHAPS and Tris （Sigma, USA）; WCX-2 （Ciphergen, USA）. Ultra-high speed hypothermia centrifuger （Bechman, USA）; Rotary tissue microtome （Keuca, Germany）; Biochip processor and PBS II-C protein chip reader （Ciphergen, USA）. METHODS： The experiments were carried out in the Institute of Molecular Pathology, Central Laboratory, and Department of Pathology, Medical College of Chinese People＇s Armed Police Force from June 2005 to March 2006. ① Grouping and treatment： The experiments were completed in molecular pathological institute, central laboratory and pathological department. ② The rats were randomly divided into control group （n =12） and brain injury group （n =60）. Marmarou＇s weight-dropping models were duplicated at different time points in the brain injury group. In the control group, the rats were only treated by incising the skin of head top, without fixing the stainless steel hitting backup plate at the vault of skull, and obtain brain cortex for pathological and protein chip research, and they were killed after 24 hours. The rats in the brain injury group were killed at 4, 8, 12, 24 and 48 hours after model establishment. ③ Pathological observation： Longitudinal section was made on cerebral cortex, and sections of 5 μm were prepared, then stained with hematoxylin and eosin （HE）. ④Protein chip analysis： 100 mg cerebral cortex was collected from each rat, and the protein content in sample was detected with Bradford method, meanwhile, WCX-2 protein chip was used to analyze the protein spectrum. The data were automatically collected with Ciphergen proteinchip 3.0 software, and the results were analyzed using Biomarker Wizard software to compare the differences of protein spectrum in rat cortex between the groups. MAIN OUTCOME MEASURES： Results of the pathological observation of cerebral cortex and the protein spectrum analysis. RESULTS：①Pathological changes of cerebral cortex： In the control group, no necrosis and edema was observed. In the brain injury group, injures of different severity occurred at different time points; After 4 hours, focal or scattered red nerve cells could be observed, the size of some cells was increased, cytoplasm was lightly stained, and only nuclear fragments were seen; After 8 hours, the necrotic nerve cells were increased, and the number of nerve cells was reduced, astrocytes （neuronophagia） could be seen in partial cytoplasm; there was small vascular dilatation, and endothelial cell proliferation; interstitial edema, regional rarefaction lightly stained. After 12- 48 hours, the necrotic nerve cells were reduced, and astrocytes proliferated. ② Results of protein spectrum analysis： The WCX-2 experiment found that the expressions of 5 639, 3 212 and 7 536 u proteins in cerebral cortex changed after injury in the brain injury group. The peak intensity of 5 639 u protein in the brain injury group at 8 hours after injury was higher than that in the control group （P 〈 0.05）; The peak intensity of 3 212 u protein in the brain injury group at 48 hours after injury was higher than that in the control group （P 〈 0.05）; The peak intensity of 7 536 u protein at 24 hours after injury was higher than that in the control group （P 〈 0.05）. CONCLUSION： Brain injury can cause the changes of protein expression spectrum in cerebral cortex, it is suggested that brain injury can induce the expression of protein.展开更多
OBJECTIVE: To evaluate the efficacy and safety of MK-801 and its effect on lesion volume in rat models of acute brain injury.DATA SOURCES: Key terms were "stroke","brain diseases","brain injur...OBJECTIVE: To evaluate the efficacy and safety of MK-801 and its effect on lesion volume in rat models of acute brain injury.DATA SOURCES: Key terms were "stroke","brain diseases","brain injuries","brain hemorrhage, traumatic","acute brain injury","dizocilpine maleate","dizocilpine","MK-801","MK801","rat","rats","rattus" and "murine". PubMed, Cochrane library, EMBASE, the China National Knowledge Infrastructure, WanFang database, the VIP Journal Integration Platform(VJIP) and SinoMed databases were searched from their inception dates to March 2018.DATA SELECTION: Studies were selected if they reported the effects of MK-801 in experimental acute brain injury. Two investigators independently conducted literature screening, data extraction, and methodological quality assessments.OUTCOME MEASURES: The primary outcomes included lesion volume and brain edema. The secondary outcomes included behavioral assessments with the Bederson neurological grading system and the water maze test 24 hours after brain injury.RESULTS: A total of 52 studies with 2530 samples were included in the systematic review. Seventeen of these studies had a high methodological quality. Overall, the lesion volume(34 studies, n = 966, MD =-58.31, 95% CI:-66.55 to-50.07;P < 0.00001) and degree of cerebral edema(5 studies, n = 75, MD =-1.21, 95% CI:-1.50 to-0.91;P < 0.00001) were significantly decreased in the MK-801 group compared with the control group. MK-801 improved spatial cognition assessed with the water maze test(2 studies, n = 60, MD =-10.88, 95% CI:-20.75 to-1.00;P = 0.03) and neurological function 24 hours after brain injury(11 studies, n = 335, MD =-1.04, 95% CI:-1.47 to-0.60;P < 0.00001). Subgroup analysis suggested an association of reduction in lesion volume with various injury models(34 studies, n = 966, MD =-58.31, 95% CI:-66.55 to-50.07;P = 0.004). Further network analysis showed that 0–1 mg/kg MK-801 may be the optimal dose for treatment in the middle cerebral artery occlusion animal model.CONCLUSION: MK-801 effectively reduces brain lesion volume and the degree of cerebral edema in rat models of experimental acute brain injury, providing a good neuroprotective effect. Additionally, MK-801 has a good safety profile, and its mechanism of action is well known. Thus, MK-801 may be suitable for future clinical trials and applications.展开更多
The high-affinity glucocorticoid binding sites（HAGS）and the low-affinity glucocor-ticoid binding sites（LAGS）with steroid specificity were demonstrated in cerebral cytosol ofrats by using the radioligand binding as...The high-affinity glucocorticoid binding sites（HAGS）and the low-affinity glucocor-ticoid binding sites（LAGS）with steroid specificity were demonstrated in cerebral cytosol ofrats by using the radioligand binding assay.The equilibrium dissocation constant（Kd）of HAGSand LAGS were（2.78+0.71）×10<sup>-8</sup>mol/L and（2.12±1.06）×10<sup>-6</sup>mol/L respectively as esti-mated by Scatchard and Pseudoseatchard analysis.Glucocorticoid receptors（GR）in the trau-matized（left）hemisphere cytosol were decreased more significantly than those in both the con-trol（right）hemisphere cytosol at 6 h postinjury and normal brain tissue（P【0.05）,but Kd ofGR showed no significant changes.GR of liver cytosol at 6h postinjury were more markedly de-creased than normal hepatic cytosol,but Kd of GR underwent no significant changes.These da-ta demonstrate that high-dose glucocorticoid（GC）used in the treatment of traumatic brain ede-ma might maintain target-cell reactions by increasing the production of GC receptor complexesand is most likely to be mediated by LAGS.展开更多
This study used electroacupuncture at Renzhong （DU26） and Baihui （DU20） in a rat model of cerebral ischemia/reperfusion injury. Neurological deficit scores, western blotting, and reverse transcription-PCR results ...This study used electroacupuncture at Renzhong （DU26） and Baihui （DU20） in a rat model of cerebral ischemia/reperfusion injury. Neurological deficit scores, western blotting, and reverse transcription-PCR results demonstrated that electroacupuncture markedly reduced neurological deficits, decreased corpus striatum aquaporin-4 protein and mRNA expression, and relieved damage to the blood-brain barrier in a rat model of cerebral ischemia/reperfusion injury. These results suggest that electroacupuncture most likely protects the blood-brain barrier by regulating aquaporin-4 expression following cerebral ischemia/reperfusion injury.展开更多
BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncert...BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.展开更多
To investigate the protective effect of dl 3 n butylphthalide (NBP) as an anti cerebral ischemic drug on brain damage 24?h after closed head injury in mice Methods Closed head injury was induced by dropping a 50...To investigate the protective effect of dl 3 n butylphthalide (NBP) as an anti cerebral ischemic drug on brain damage 24?h after closed head injury in mice Methods Closed head injury was induced by dropping a 50 g weight from a height of 18?cm on a metal impounder resting on the parietal bone in mice Results The neurotraumatic model induced impair^ment of memory function, significant cerebral edema, and disruption of the blood brain barrier dl 3 n butylphthalide (50?mg·kg 1 ) given intraperitoneally 5 minutes and 60 minutes after the onset of closed head injury was found to attenuate the impairment of memory function ( P <0 05), alleviate brain edema in the injured cerebral cortex ( P <0 05), and reduce extravasation of plasma protein bound to Evans blue dye by 63 5% ( P <0 01) NBP was also shown to increase the activity of choline acetyltransferase in the injured cortex to 0 83±0 21?ng·min 1 ·mg 1 ( P <0 01, compared with 0 48±0 14?ng·min 1 ·mg 1 of vehicle group) Conclusion NBP provides therapeutic response in experimental closed head injury展开更多
Objective:To observe the effect of Cassia o btusifolial extract on rats of traumatic brain injury.Methods:The rats were randomly divided into 4 groups,traumatic brain injur(TBI)group,sham operation group(SHAM)group,(C...Objective:To observe the effect of Cassia o btusifolial extract on rats of traumatic brain injury.Methods:The rats were randomly divided into 4 groups,traumatic brain injur(TBI)group,sham operation group(SHAM)group,(COB-H20 g/kg、COB-L10 g/kg)of Cassia extract groups,They were subjected to the modified Feeney's weight-drop model.sham group fake open skull window only,Cassia o btusifolial extract were given by intragastric administration and the rats were given distilled water instead as TBI and SHAM.The behavioral test was performed by Balance beam,TNF-αand IL-6 level was detected by ELASA method in serum on rats of TBI,The NSE positive cells near the region of injury was ascertainde by measuring in rats of TBI,and Western blot was used to detect the expressions of PI3K in rat brain tissues.Results:Both of Cassia extract groups and TBI traversed the beam significantly quicker than sham group at 3 time points before and after injury(P<0.01),and both of COB groups traversed the beam significantly shorter than TBI(P<0.05).The serum TNF-αand IL-6 content in TBI and Both of COB groups were significantly higher than sham group at 6,24,60h(P<0.01),To compare with the TBI group,the serum TNF-αand IL-6 content in the both of COB groups were significantly decreased respectively at the time 6,24 and 60 hours,The overall level gradually decreased at 24 h,but increased slightly at 60 h.Immunohistochemical method revealed that NSE was lowered dramaticly in sham and both of COB groups(P<0.05),but it was more efficient in both of COB groups compared to TBI group(P<0.05).the expressions of PI3 protein of the TBI group was decreased observbly than sham group(P<0.05),but COB-H group was inecreased significantly than TBI group same as sham group(P<0.05).Conclusion:Cassia o btusifolial extract can improve neurol function,increasing NSE positive cells and the expressions of PI3 protein lever.展开更多
基金the National Natural Science Foundation of China,No.30471934
文摘BACKGROUND： Mechanical injury can cause the changes of polygene expression spectrum in rat cerebral cortical nerve cells, and then result in the changes of intracellular protein expression. At present, dielectrophoresis is combined with mass spectrum technique to detect the expression of different proteins in rat cortex after brain injury, but the protein chip technique requires further investigation. OBJECTIVE： To analyze the differences of protein expression spectrum in rat cerebral cortex before and after closed traumatic brain injury using WCX-2 protein chip technique. DESIGN： A randomized controlled animal experiment. SETTING： Training Division of the Medical College of Chinese People＇s Armed Police Force. MATERIALS： Seventy-two male SD rats of clean degree, 350 - 450 g, were provided by the Experimental Animal Center, Academy of Military Medical Sciences of Chinese PLA. Urea, trifluoroacetic acid, CHAPS and Tris （Sigma, USA）; WCX-2 （Ciphergen, USA）. Ultra-high speed hypothermia centrifuger （Bechman, USA）; Rotary tissue microtome （Keuca, Germany）; Biochip processor and PBS II-C protein chip reader （Ciphergen, USA）. METHODS： The experiments were carried out in the Institute of Molecular Pathology, Central Laboratory, and Department of Pathology, Medical College of Chinese People＇s Armed Police Force from June 2005 to March 2006. ① Grouping and treatment： The experiments were completed in molecular pathological institute, central laboratory and pathological department. ② The rats were randomly divided into control group （n =12） and brain injury group （n =60）. Marmarou＇s weight-dropping models were duplicated at different time points in the brain injury group. In the control group, the rats were only treated by incising the skin of head top, without fixing the stainless steel hitting backup plate at the vault of skull, and obtain brain cortex for pathological and protein chip research, and they were killed after 24 hours. The rats in the brain injury group were killed at 4, 8, 12, 24 and 48 hours after model establishment. ③ Pathological observation： Longitudinal section was made on cerebral cortex, and sections of 5 μm were prepared, then stained with hematoxylin and eosin （HE）. ④Protein chip analysis： 100 mg cerebral cortex was collected from each rat, and the protein content in sample was detected with Bradford method, meanwhile, WCX-2 protein chip was used to analyze the protein spectrum. The data were automatically collected with Ciphergen proteinchip 3.0 software, and the results were analyzed using Biomarker Wizard software to compare the differences of protein spectrum in rat cortex between the groups. MAIN OUTCOME MEASURES： Results of the pathological observation of cerebral cortex and the protein spectrum analysis. RESULTS：①Pathological changes of cerebral cortex： In the control group, no necrosis and edema was observed. In the brain injury group, injures of different severity occurred at different time points; After 4 hours, focal or scattered red nerve cells could be observed, the size of some cells was increased, cytoplasm was lightly stained, and only nuclear fragments were seen; After 8 hours, the necrotic nerve cells were increased, and the number of nerve cells was reduced, astrocytes （neuronophagia） could be seen in partial cytoplasm; there was small vascular dilatation, and endothelial cell proliferation; interstitial edema, regional rarefaction lightly stained. After 12- 48 hours, the necrotic nerve cells were reduced, and astrocytes proliferated. ② Results of protein spectrum analysis： The WCX-2 experiment found that the expressions of 5 639, 3 212 and 7 536 u proteins in cerebral cortex changed after injury in the brain injury group. The peak intensity of 5 639 u protein in the brain injury group at 8 hours after injury was higher than that in the control group （P 〈 0.05）; The peak intensity of 3 212 u protein in the brain injury group at 48 hours after injury was higher than that in the control group （P 〈 0.05）; The peak intensity of 7 536 u protein at 24 hours after injury was higher than that in the control group （P 〈 0.05）. CONCLUSION： Brain injury can cause the changes of protein expression spectrum in cerebral cortex, it is suggested that brain injury can induce the expression of protein.
基金supported by the National Natural Science Foundation of China,No.81822050(to QQL),81873321(to HX),81673990(to QQL),81330085(to QS),81730107(to YJW)the Shanghai Municipal Health and Family Planning Commission TCM Research Project of China,No.2018JP014(to HX)+4 种基金the Three-Year Action Plan to Promote Clinical Skills and Clinical Innovation in Municipal Hospitals of China,No.16CR1017A(to YJW)the Shanghai Traditional Chinese Medicine Chronic Disease [Malignant Tumor,Bone Degenerative Disease] Clinical Medical Center of China,No.2017ZZ01010(to YJW)the National Ministry of Education Innovation Team of China,No.IRT1270(to YJW)the Innovation Team of Key Fields of the Ministry of Science and Technology of China,No.2015RA4002(to YJW)the Outstanding Principle Investigator Project of Guanghua Hospital,Changning District,Shanghai,China,No.2016-01(to QS),2016-06(to YJW)
文摘OBJECTIVE: To evaluate the efficacy and safety of MK-801 and its effect on lesion volume in rat models of acute brain injury.DATA SOURCES: Key terms were "stroke","brain diseases","brain injuries","brain hemorrhage, traumatic","acute brain injury","dizocilpine maleate","dizocilpine","MK-801","MK801","rat","rats","rattus" and "murine". PubMed, Cochrane library, EMBASE, the China National Knowledge Infrastructure, WanFang database, the VIP Journal Integration Platform(VJIP) and SinoMed databases were searched from their inception dates to March 2018.DATA SELECTION: Studies were selected if they reported the effects of MK-801 in experimental acute brain injury. Two investigators independently conducted literature screening, data extraction, and methodological quality assessments.OUTCOME MEASURES: The primary outcomes included lesion volume and brain edema. The secondary outcomes included behavioral assessments with the Bederson neurological grading system and the water maze test 24 hours after brain injury.RESULTS: A total of 52 studies with 2530 samples were included in the systematic review. Seventeen of these studies had a high methodological quality. Overall, the lesion volume(34 studies, n = 966, MD =-58.31, 95% CI:-66.55 to-50.07;P < 0.00001) and degree of cerebral edema(5 studies, n = 75, MD =-1.21, 95% CI:-1.50 to-0.91;P < 0.00001) were significantly decreased in the MK-801 group compared with the control group. MK-801 improved spatial cognition assessed with the water maze test(2 studies, n = 60, MD =-10.88, 95% CI:-20.75 to-1.00;P = 0.03) and neurological function 24 hours after brain injury(11 studies, n = 335, MD =-1.04, 95% CI:-1.47 to-0.60;P < 0.00001). Subgroup analysis suggested an association of reduction in lesion volume with various injury models(34 studies, n = 966, MD =-58.31, 95% CI:-66.55 to-50.07;P = 0.004). Further network analysis showed that 0–1 mg/kg MK-801 may be the optimal dose for treatment in the middle cerebral artery occlusion animal model.CONCLUSION: MK-801 effectively reduces brain lesion volume and the degree of cerebral edema in rat models of experimental acute brain injury, providing a good neuroprotective effect. Additionally, MK-801 has a good safety profile, and its mechanism of action is well known. Thus, MK-801 may be suitable for future clinical trials and applications.
文摘The high-affinity glucocorticoid binding sites（HAGS）and the low-affinity glucocor-ticoid binding sites（LAGS）with steroid specificity were demonstrated in cerebral cytosol ofrats by using the radioligand binding assay.The equilibrium dissocation constant（Kd）of HAGSand LAGS were（2.78+0.71）×10<sup>-8</sup>mol/L and（2.12±1.06）×10<sup>-6</sup>mol/L respectively as esti-mated by Scatchard and Pseudoseatchard analysis.Glucocorticoid receptors（GR）in the trau-matized（left）hemisphere cytosol were decreased more significantly than those in both the con-trol（right）hemisphere cytosol at 6 h postinjury and normal brain tissue（P【0.05）,but Kd ofGR showed no significant changes.GR of liver cytosol at 6h postinjury were more markedly de-creased than normal hepatic cytosol,but Kd of GR underwent no significant changes.These da-ta demonstrate that high-dose glucocorticoid（GC）used in the treatment of traumatic brain ede-ma might maintain target-cell reactions by increasing the production of GC receptor complexesand is most likely to be mediated by LAGS.
基金funded by the National NaturalScience Foundation of China (Youth), No. 81001556
文摘This study used electroacupuncture at Renzhong （DU26） and Baihui （DU20） in a rat model of cerebral ischemia/reperfusion injury. Neurological deficit scores, western blotting, and reverse transcription-PCR results demonstrated that electroacupuncture markedly reduced neurological deficits, decreased corpus striatum aquaporin-4 protein and mRNA expression, and relieved damage to the blood-brain barrier in a rat model of cerebral ischemia/reperfusion injury. These results suggest that electroacupuncture most likely protects the blood-brain barrier by regulating aquaporin-4 expression following cerebral ischemia/reperfusion injury.
基金Supported by: the Foundation Program of Shandong Heatth Department, No. 2001CAICKAF
文摘BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.
基金TheworkwassupportedbythegrantofStateScienceandTechnologyCommissionofChina (No .94 ZD 0 1 )
文摘To investigate the protective effect of dl 3 n butylphthalide (NBP) as an anti cerebral ischemic drug on brain damage 24?h after closed head injury in mice Methods Closed head injury was induced by dropping a 50 g weight from a height of 18?cm on a metal impounder resting on the parietal bone in mice Results The neurotraumatic model induced impair^ment of memory function, significant cerebral edema, and disruption of the blood brain barrier dl 3 n butylphthalide (50?mg·kg 1 ) given intraperitoneally 5 minutes and 60 minutes after the onset of closed head injury was found to attenuate the impairment of memory function ( P <0 05), alleviate brain edema in the injured cerebral cortex ( P <0 05), and reduce extravasation of plasma protein bound to Evans blue dye by 63 5% ( P <0 01) NBP was also shown to increase the activity of choline acetyltransferase in the injured cortex to 0 83±0 21?ng·min 1 ·mg 1 ( P <0 01, compared with 0 48±0 14?ng·min 1 ·mg 1 of vehicle group) Conclusion NBP provides therapeutic response in experimental closed head injury
基金Innovative and Entrepreneurship Training Foundation of Hainan Medical college students at 2016(No.HYCX2016083)Innovative and Entrepreneurship Training Foundation of Hainan province students at 2017(No.2017126)
文摘Objective:To observe the effect of Cassia o btusifolial extract on rats of traumatic brain injury.Methods:The rats were randomly divided into 4 groups,traumatic brain injur(TBI)group,sham operation group(SHAM)group,(COB-H20 g/kg、COB-L10 g/kg)of Cassia extract groups,They were subjected to the modified Feeney's weight-drop model.sham group fake open skull window only,Cassia o btusifolial extract were given by intragastric administration and the rats were given distilled water instead as TBI and SHAM.The behavioral test was performed by Balance beam,TNF-αand IL-6 level was detected by ELASA method in serum on rats of TBI,The NSE positive cells near the region of injury was ascertainde by measuring in rats of TBI,and Western blot was used to detect the expressions of PI3K in rat brain tissues.Results:Both of Cassia extract groups and TBI traversed the beam significantly quicker than sham group at 3 time points before and after injury(P<0.01),and both of COB groups traversed the beam significantly shorter than TBI(P<0.05).The serum TNF-αand IL-6 content in TBI and Both of COB groups were significantly higher than sham group at 6,24,60h(P<0.01),To compare with the TBI group,the serum TNF-αand IL-6 content in the both of COB groups were significantly decreased respectively at the time 6,24 and 60 hours,The overall level gradually decreased at 24 h,but increased slightly at 60 h.Immunohistochemical method revealed that NSE was lowered dramaticly in sham and both of COB groups(P<0.05),but it was more efficient in both of COB groups compared to TBI group(P<0.05).the expressions of PI3 protein of the TBI group was decreased observbly than sham group(P<0.05),but COB-H group was inecreased significantly than TBI group same as sham group(P<0.05).Conclusion:Cassia o btusifolial extract can improve neurol function,increasing NSE positive cells and the expressions of PI3 protein lever.
