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This study investigated the effect of Xiaoxuming Decoction(XXMD) on the activation of astrocytes after cerebral ischemia/reperfusion(I/R) injury. The model of cerebral IR injury was established using the middle cerebral artery occlusion method. Fluorocitrate(FC), an inhibitor of astrocyte activation, was applied to inhibit astrocyte activation. Rats were randomly divided into a sham group, a model group, a XXMD group, a XXMD+FC group, and a XXMD+Vehicle group. Neurobehavioral changes at 24 hours after cerebral IR injury, cerebral infarction, histopathological changes observed through HE staining, submicroscopic structure of astrocytes observed through transmission electron microscopy, fluorescence intensity of glial fibrillary acidic protein(GFAP) and thrombospondin 1(TSP1) measured through immunofluorescence, and expression of GFAP and TSP1 in brain tissue measured through Western blot were evaluated in rats from each group. The experimental results showed that neurobehavioral scores and cerebral infarct area significantly increased in the model group. The XXMD group, the XXMD+FC group, and the XXMD+Vehicle group all alleviated neurobehavioral changes in rats. The pathological changes in the brain were evident in the model group, while the XXMD group, the XXMD+FC group, and the XXMD+Vehicle group exhibited milder cerebral IR injury in rats. The submicroscopic structure of astrocytes in the model group showed significant swelling, whereas the XXMD group, the XXMD+FC group, and XXMD+Vehicle group protected the submicroscopic structure of astrocytes. The fluorescence intensity and protein expression of GFAP and TSP1 increased in the model group compared with those in the sham group. However, the XXMD group, the XXMD+FC group, and XXMD+Vehicle group all down-regulated the expression of GFAP and TSP1. The combination of XXMD and FC showed a more pronounced effect. These results indicate that XXMD can improve cerebral IR injury, possibly by inhibiting astrocyte activation and down-regulating the expression of GFAP and TSP1.
Subject(s)
Rats , Animals , Astrocytes , Brain Ischemia/metabolism , Brain , Reperfusion Injury/metabolism , Infarction, Middle Cerebral ArteryABSTRACT
ObjectiveTo investigate the effects of Anmeidan （AMD） on neuronal structure and neuronal marker protein expression in the hippocampal CA1 region of sleep-deprived （SD） rats. MethodRats were randomly divided into control group， model group， an AMD group （9.09 g·kg-1·d-1）， and melatonin group （0.27 g·kg-1·d-1）. Rats in the control group and the model group received equal volumes of physiologicol saline. The SD model was induced by the self-made sleep deprivation box for four weeks. Ethovision XT system detected and analyzed the spontaneous behaviors of rats. The histomorphology of neurons in the hippocampal CA1 region was observed by hematoxylin-eosin （HE） staining and Nissl staining， and the changes in Nissl bodies were observed by Nissl staining. The ultrastructure of hippocampal cells was observed by transmission electron microscopy （TEM）. Immunohistochemistry was used to detect the expression of glial fibrillary acidic protein （GFAP）， microtubule-associated protein 2 （MAP2）， nestin， and neuronal nuclei （NeuN） in the CA1 region. ResultCompared with the control group， the model group showed longer distance， increased average activity speed， cumulative duration， average body fill， and higher activity frequency （P<0.01）. Besides， the neurons in the CA1 region were reduced in number with disorganized arrangement， wrinkled nuclei， deeply stained cytoplasm， reduced Nissl bodies， swollen and deformed mitochondria， shortened cristae， and swollen Golgi vesicles. Furthermore， the mean integral absorbance （IA） value of GFAP increased and those of MAP2， nestin， and NeuN decreased （P<0.01）. Compared with the model group， the AMD group showed shortened distance traveled， lower average activity speed， shorter cumulative duration， decreased average body fill， and reduced activity frequency （P<0.05， P<0.01）. Moreover， the neurons in the CA1 region were relieved from damage with increased cell number， clear nuclei and cytoplasm， increased Nissl bodies， and relieved mitochondrial damage. The IA value of GFAP decreased and those of MAP2， nestin， and NeuN increased （P<0.05， P<0.01）. ConclusionAMD can improve structural damage of neurons in the hippocampal CA1 region of sleep-deprived rats， which may be achieved by decreasing GFAP expression and increasing MAP2， nestin， and NeuN expression.
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Objective: To investigate the possible role of astrocytes after brain infarction in stroke-prone, spontaneously hypertensive (SHR-SP) rats and the association with angiogenesis and the architecture. Methods: We maintained SHR-SP rats on high sodium water starting to accelerate the stroke onset. The 3D quantification of microvasculatures (diameter, branch number) by cofocal microscope after FITC-dextran was injected into the rats via the left femoral vein. Glial fibrillary acidic protein (GFAP) expression and microvessel density (MVD) using counting the number of factor -positive endothelial cells were evaluated by immunofluorescence and immunohistochemistry, respectively. Results: Cerebral infarction occurred at week 7 after high sodium water intake (13 g/L NaCl) in SHR-SP group. When compared with the non-infarcted contralateral hemisphere and SHR-SP on normal sodium intake and WKY rats, GFAP expression and MVD were significantly increased, respectively, and the diameter and the branch number of vessels were decreased, respectively, in cerebral infarcts with boundary zones of SHR-SP rats (P<0.01). Linear correlation analysis showed that GFAP expression was positively correlated with MVD and the diameter and the branch number of vessels in cerebral infarcts in SHR-SP (P<0.01). Conclusion: Astrocytes hyperplasia may be associated with increased regional angiogenesis and the changes of architecture in SHR-SP rats with high sodium water (13 g/L NaCl) that induces focal cerebral infarcts.
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Objective: To investigate the effect of aquaporin 4(AQP4)in neuropathic pain and explore the rela- tionship with the activation of spinal astrocytes and release of proinflammatory cytokines. Methods: The effect of AQP4 gene knockout(KO)on the pain-related behavior was investigated using the sciatic nerve branch injury model(SNI)of AQP4 KO and wild type(WT)mice. The expression of astrocyte activation-related protein,glial fibrillary acidic protein(GFAP),and the level of proinflammatory cytokines,TNF-α and IL-6,all in the mouse spinal cord samples,were detect- ed by Western blot(WB)and ELISA,respectively. Results: After SNI surgery,compared with the WT group,a signifi- cant attenuation in mechanical allodynia was found in the KO group(P<0.01),however,no difference was detected be- tween two sham groups(Sham)of WT and KO mice(P>0.05). These results indicated that the AQP4 gene knockout re- lieved neuropathic pain. Fouteen days after SNI surgery,WB results showed that the GFAP level in mouse spinal cord was significantly higher in the WT-SNI group than in the WT-Sham group(P<0.01),whereas the GFAP level in the KOSNI group was significantly lower than that in the WT-SNI group(P<0.01). These results indicated that AQP4 KO inhib- ited activation of spinal astrocytes in SNI model mice. In addition,14 days after SNI surgery,ELISA results showed that the levels of mouse spinal cord proinflammatory cytokines,TNF-α and IL-6 in the WT-SNI group were significantly high- er than those in the WT-Sham group(P<0.05 and P<0.01,respectively),whereas the levels of TNF-α and IL-6 in the KO-SNI group were significantly lower than those in the WT-SNI group(P<0.05 and P<0.01,respectively). These re- sults indicated that AQP4 KO inhibited the level of mouse spinal cord proinflammatory cytokines in SNI model mice. Conclusion: The AQP4 gene knockout may relieve the neuropathic pain via the inhibition of the astrocyte activation and proinflammatory cytokine release.
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Objective: To detect the effects of propofol on rat hippocampal astrocytes and clarify its mechanism. Methods: According to the time after propofol injection, twenty-four SD rats were randomly divided into three groups, i. e. 0 min, 45 min and 90 min group. Rats were administrated intraperitoneally with propofol (10 mg/mL, 100 mg/kg body weight). The levels of glial fibrillary acidic protein (GFAP) and S100β mRNA in rat hippocampus were evaluated by realtime PCR. And cell viabilities and levels of GFAP mRNA were examined in primary cultured hippocampal astrocytes induced by 10 μmol/L propofol with or without 10 μmol/L extracellular signal-regulated kinase (ERK) inhibitor PD98059 pretreatment. Results: The mRNA levels of GFAP in the hippocampal tissue were (1.32±0.12) times (P=0.000) and (1.12±0.09) times (P=0.012) that in 0 min group, respectively, 45 min and 90 min after injection of propofol. The mRNA levels of S100β in the hippocampal tissue were (1.14±0.11) times (P=0.005) and (1.05±0.10) times (P=0.284) that in 0 min group, respectively, 45 min and 90 min after injection of propofol. The mRNA levels of GFAP and S100β were timedependently altered, first increasing, and then decreasing. In vitro, the cell viabilities (P=0.041) and levels of GFAP mRNA (P=0.026) in primary cultured hippocampal astrocytes were significantly elevated after propofol treatment, and these effects of propofol were reversed by ERK inhibitor PD98059. Conclusion: Propofol time-dependently upregulated the expression of GFAP and S100β via ERK signaling pathway in rat hippocampal astrocytes, so as to activate astrocytes.
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Objective·To detect the effects of propofol on rat hippocampal astrocytes and clarify its mechanism.Methods·According to the time after propofol injection,twenty-four SD rats were randomly divided into three groups,i.e.0 min,45 min and 90 min group.Rats were administrated intraperitoneally with propofol (10 mg/mL,100 mg/kg body weight).The levels of glial fibrillary acidic protein (GFAP) and S100β mRNA in rat hippocampus were evaluated by realtime PCR.And cell viabilities and levels of GFAP mRNA were examined in primary cultured hippocampal astrocytes induced by 10 μmol/L propofol with or without 10 μmol/L extracellular signal-regulated kinase (ERK) inhibitor PD98059 pretreatment.Results·The mRNA levels of GFAP in the hippocampal tissue were (1.32±0.12) times (P=0.000) and (1.12±0.09) times (P=0.012) that in 0 min group,respectively,45 min and 90 min after injection of propofol.The mRNA levels of S100β in the hippocampal tissue were (1.14±0.11) times (P=0.005) and (1.05±0.10)times (P=0.284) that in 0 min group,respectively,45 min and 90 min after injection of propofol.The mRNA levels of GFAP and S100β were timedependently altered,first increasing,and then decreasing.In vitro,the cell viabilities (P=0.041) and levels of GFAP mRNA (P=0.026) in primary cultured hippocampal astrocytes were significantly elevated after propofol treatment,and these effects of propofol were reversed by ERK inhibitor PD98059.Conclusion·Propofol time-dependently upregulated the expression of GFAP and S100β via ERK signaling pathway in rat hippocampal astrocytes,so as to activate astrocytes.
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OBJECTIVE@#To observe the effects of treatment on the ultrastructure of olfactory bulb and the expression of substantia nigra glial fibrillary acidic protein (GFAP) in mice with Parkinson's disease (PD) induced by lipopolysaccharide (LPS), and to provide methods and evidence for early prevention and treatment of PD.@*METHODS@#Forty C57BL/6 male mice were randomly divided into a blank group, a model group, an electroacupuncture (EA) group and a medication group, 10 mice in each one. The mice in the model group, EA group and medication group were treated with 30-day nasal perfusion of LPS to establish PD model. From the first day of model establishment, the mice in the EA group were treated with electroacupuncture at bilateral "Yingxiang" (LI 20) and "Yintang" (GV 29) for 20 min, once a day; 5-day treatment was taken as one session, and 4 sessions were given with an interval of 2 days between sessions. The mice in the medication group were treated with intraperitoneal injection of L-DOPA, 10 mg/mL, once a day; 5-day treatment was taken as one session, and 4 sessions were given with an interval of 2 days between sessions. After treatment, the behavioristics changes were observed by using footprint analysis and swimming test score; the ultrastructure of olfactory bulb was observed by using transmission electron microscopy; the expression of GFAP in substantia nigra was measured by using western blot method.@*RESULTS@#① After model establishment, the mice in the model group, the EA group and medication group showed significant symptoms of quiver and fear of chill, and the BMI was significantly lower than that in the blank group (all 0.05). ③ After treatment, the footprint and swimming time in the model group were significantly lower than that in the blank group (both <0.01); the footprint and swimming time in the EA group and medication group were significantly higher than those in the model group (all <0.01).④ After treatment, compared with the blank group, the organelles and ultrastructure of olfactory bulb in the model group were significantly improved; the ultrastructure of olfactory bulb in the EA group was improved compared with that in the model group. ⑤ After treatment, the expression of substantia nigra GFAP in the model group was significantly higher than that in the blank group (<0.01); the expression of substantia nigra GFAP in the EA group and medication group was significantly lower than that in the model group (both <0.05).@*CONCLUSION@#The early treatment of can improve behavioral disorders in LPS-induced early PD mice, and the mechanism may be related to the regulation of olfactory disorders and the expression of GFAP in substantia nigra.
Subject(s)
Animals , Male , Rats , Electroacupuncture , Glial Fibrillary Acidic Protein , Mice, Inbred C57BL , Olfactory Bulb , Parkinson Disease , Rats, Sprague-DawleyABSTRACT
Objective To investigate the early diagnosis value of arterial blood gas analysis , neuron specific enolase and serum glial fibrillary acidic protein in brain injury of premature infant. Methods In the study, 95 premature infants admitted in our hospital were enrolled. 45 premature infants with brain injury were selected as experimental group. 50 premature infants without brain injury were selected as control group. All patients received arterial blood gas analysis , NSE and GFAP on the 1st day and 7th day after birth. Results There is statistically significant difference between the experimental group and the control group on the 1st day after birth in terms of pCO2, pH, BE and lactic acid (P<0.05). In experimental group, there is statistically significant difference between the 1st day and 7th day after birth in terms of pCO2, pH, BE and lactic acid (P < 0.05). The NSE and GFAP levels had statistically significant difference between the experimental group and the control group on the 1st day and 7th day after birth(P < 0.01); the NSE levels of experimental group had statistically significant difference between the 1st day and 7th day after birth (P < 0.05); The GFAP levels of experimental group had statistically significant difference between the 1st day and 7th day after birth (P < 0.01). Conclusion pCO2, NSE and GFAP levels are correlated with brain damage in premature infants in early stage. This could provide evidence of early diagnosis for brain injury in preterm infants.
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Diabetes mellitus can cause central nervous system disorder that is summarized as diabetic encephalopathy, which manifests in cognitive dysfunction and other mental illnesses. Astrocyte ,with a huge number and extensive functions,is an im?portant part of the central nervous system. Morphological and functional changes in astrocyte have been observed in diabetes mellitus , which involve the quantity,the expression of neurotransmitters and relative transporters,the activity of enzyme,the storage of glyco?gen and the intercellular connection and communication.
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Diabetes mellitus can cause central nervous system disorder that is summarized as diabetic encephalopathy, which manifests in cognitive dysfunction and other mental illnesses. Astrocyte, with a huge number and extensive functions, is an important part of the central nervous system. Morphological and functional changes in astrocyte have been observed in diabetes mellitus, which involve the quantity, the expression of neurotransmitters and relative transporters, the activity of enzyme, the storage of glycogen and the intercellular connection and communication.
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Toxocariasis is a soil-transmitted helminthozoonosis due to infection of humans by larvae of Toxocara canis. The disease could produce cognitive and behavioral disturbances especially in children. Meanwhile, in our modern era, the incidence of immunosuppression has been progressively increasing due to increased incidence of malignancy as well as increased use of immunosuppressive agents. The present study aimed at comparing some of the pathological and immunological alterations in the brain of normal and immunosuppressed mice experimentally infected with T. canis. Therefore, 180 Swiss albino mice were divided into 4 groups including normal (control) group, immunocompetent T. canis-infected group, immunosuppressed group (control), and immunosuppressed infected group. Infected mice were subjected to larval counts in the brain, and the brains from all mice were assessed for histopathological changes, astrogliosis, and IL-5 mRNA expression levels in brain tissues. The results showed that under immunosuppression, there were significant increase in brain larval counts, significant enhancement of reactive gliosis, and significant reduction in IL-5 mRNA expression. All these changes were maximal in the chronic stage of infection. In conclusion, the immunopathological alterations in the brains of infected animals were progressive over time, and were exaggerated under the effect of immunosuppression as did the intensity of cerebral infection.
Subject(s)
Animals , Female , Male , Mice , Brain/pathology , Disease Models, Animal , Gene Expression Profiling , Histocytochemistry , Immunocompromised Host , Immunohistochemistry , Interleukin-5/genetics , Parasite Load , Toxocara canis/immunology , Toxocariasis/immunologyABSTRACT
Toxocariasis is a soil-transmitted helminthozoonosis due to infection of humans by larvae of Toxocara canis. The disease could produce cognitive and behavioral disturbances especially in children. Meanwhile, in our modern era, the incidence of immunosuppression has been progressively increasing due to increased incidence of malignancy as well as increased use of immunosuppressive agents. The present study aimed at comparing some of the pathological and immunological alterations in the brain of normal and immunosuppressed mice experimentally infected with T. canis. Therefore, 180 Swiss albino mice were divided into 4 groups including normal (control) group, immunocompetent T. canis-infected group, immunosuppressed group (control), and immunosuppressed infected group. Infected mice were subjected to larval counts in the brain, and the brains from all mice were assessed for histopathological changes, astrogliosis, and IL-5 mRNA expression levels in brain tissues. The results showed that under immunosuppression, there were significant increase in brain larval counts, significant enhancement of reactive gliosis, and significant reduction in IL-5 mRNA expression. All these changes were maximal in the chronic stage of infection. In conclusion, the immunopathological alterations in the brains of infected animals were progressive over time, and were exaggerated under the effect of immunosuppression as did the intensity of cerebral infection.
Subject(s)
Animals , Female , Male , Mice , Brain/pathology , Disease Models, Animal , Gene Expression Profiling , Histocytochemistry , Immunocompromised Host , Immunohistochemistry , Interleukin-5/genetics , Parasite Load , Toxocara canis/immunology , Toxocariasis/immunologyABSTRACT
@#The nature and functions of astrocytes (AS)， the pathological changes and roles of AS after spinal cord injury， the experimental methods of inhibiting AS proliferation and glial scar formation， and so on, were reviewed. AS beneficially affects repairing injured spinal cord at different periods of differentiation. However， adult AS secreting the factors formed the chemical glial barrier which severely affects nerve regeneration and hinders axon extension. Because of the static， activated and proliferative AS tending to coexist after spinal cord injury， and complex factors of barrier formation， the current approach taken by a single method is difficult to effectively control the AS proliferation and glial scar formation.
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@#Objective To observe the effect of chronic cerebral hypoperfusion on abilities of learning and memory and astrocytes in old rats. Methods 50 Wistar rats were randomly divided into the sham group and model group with 25 animals in each group. All animals were assessed with Morris water maze to test the changes of abilities of learning and memory. The expressions of glial fibrillary acidic protein (GFAP) in the frontal lobe and hippocampus were observed immunohistochemically. Results Compared with the sham group, the scores of Morris water maze decreased in the model group, while the astrocytes marked by GFAP proliferated and enlarged significantly. Conclusion Proliferation and morphological changes of astrocytes are involved in pathological mechanism of chronic cerebral hypoperfusion, which might be associated with the decrease of ability of learning and memory.
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@#ObjectiveTo observe the relationship between astrocytes and neurons in rat's medulla oblongata after exposed to 8Hz, 90dB/130dB infrasound for different times. MethodsRats were exposed to 8Hz, 90dB/130dB infrasound for 2 hours per day.At the 1st,7th,12th,21th and 28th day, the expression of glial fibrillary acidic protein (GFAP) and Fos in medulla oblongata were detected using double-labling immunohistochemical method.Results GFAP-positive astrocytes and Fos-positive neurons were increased after exposure for one time. They showed similar topographic localization and formed close relationship. Their number increased as the exposure times increasing, and decreased gradually after 14 days. The reaction of 130dB group was stronger than that of 90dB group.Conclusions 8Hz, 90dB/130dB infrasound can activate both astrocytes and neurons in rats' medulla oblongata which might participate and regulate the response to infrasound.
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This is a rare case of cerebral metastasis from malignant fibrous histiocytoma(MFH) of the soft tissue. A 62-year-old man underwent craniotomy for resection of multiple intracerebral masses under the impression of metastatic brain tumor with unknown primary site. Preoperative investigation failed to detect any extracranial lesion. At six months after the operation and whole brain radiotherapy, right shoulder mass was detected to grow and excised. Specimen from the brain and shoulder lesions revealed identical pathological findings of malignant fibrous histiocytoma except existence of glial fibrillary acidic protein(GFAP)-positive cells only in brain lesions. Palliative radiotherapy was performed for subsequently developing metastatic lesions in skeletal system. At twelve months after initial diagnosis recurrent lesion at right shoulder was detected and chemotherapy is given. This case is unique because metastatic brain lesion from MFH is rare and also cerebral metastasis as an initial manifestaion of MFH has not been reported before. Another important finding is that there was expression of GFAP only in brain lesions but not in extracranial primary site lesion. Although the presence of GFAP-positive cells is thought as one of characteristic histological findings of primary intracrainal MFH, our observation supports the hypothesis that GFAP-positive cells in primary intracranial MFH may be nonneoplastic astrocytes secondarily involved by MFH.
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Humans , Middle Aged , Astrocytes , Brain , Brain Neoplasms , Craniotomy , Diagnosis , Drug Therapy , Histiocytoma, Malignant Fibrous , Neoplasm Metastasis , Radiotherapy , ShoulderABSTRACT
Ependymal cells line the surface of cerebral ventricles. They do not regenerate after they are fully matured and have a limited response to injury. In hydrocephalus, the expansile force of the ventricular wall is applied to ependymal cells and causes cell deformity to some degree. As it is known that the intermediate filaments of a cell act as a framework that resists changes in cellular shape, there may be some detectable changes of intermediate filaments of ependymal cells in hydrocephalus. In developing ependymal cells, it is also unclear if there are any changes to intermediate filaments in hydrocephalus. Developing ependymal cells are known to lose their immunoreactivity to glial fibrillary acidic protein (GFAP), a kind of intermediate filaments which exist in some neuroglial cells. We experimentally induced congenital and postnatal hydrocephalus and investigated the changes of immunore-activity against GFAP as well as the ultrastuctures of rat ependymal cells in both types of hydrocephalus. To induce congenital hydrocephalus, 40 mg/kg of ethylenethiourea (ETU) was orally administered to pregnant rats on the 15th day after conception. Tissues taken from fetuses on the 17th day, from newborn rats immediately after birth, and from rats of 1 week and 2 weeks after birth were obtained and processed for immunohistochemistry for GFAP and electron microscopy. Postnatal hydrocephalus was induced by injecting kaolin suspension into the subarachnoid space of 15-day-old rats. Ependymal tissues were obtained and processed for immunohistochemistry and electron microscopy after 1 and 2 weeks following injection. The results were as follows; 1. Congenital hydrocephalus was induced more consistently and extensively than postnatal hydrocephalus. 2. In congenital hydrocephalus, GFAP-reactive ependymal cells were found in lateral ventricles of 1-week and 2-week-old rats, while in control and postnatal hydrocephalic groups, GFAP-reactive ependymal cells were not found. GFAP-reactive cells tended to be found in clusters. 3. Electron microscopy showed ependymal cells in congenital hydrocephalus had a less marked flattening figure, scarce apical cilia, often widened regions in the intercellular gap, spaces in subependymal tissue, and different figures in mitochondria. Above all, intermediate filaments, including GFAP, increased and were irregularly arranged in ependymal cell cytoplasm in congenital hydrocephalus. Therefore, in congenitally-induced hydrocephalus, the ependymal cells appeared to have a greater responsiveness to expansile force and remained in a more premature state than postnatally-induced hydrocephalus.
Subject(s)
Animals , Humans , Infant, Newborn , Rats , Cerebral Ventricles , Cilia , Congenital Abnormalities , Cytoplasm , Ethylenethiourea , Fertilization , Fetus , Glial Fibrillary Acidic Protein , Hydrocephalus , Immunohistochemistry , Intermediate Filaments , Kaolin , Lateral Ventricles , Microscopy, Electron , Mitochondria , Neuroglia , Parturition , Subarachnoid SpaceABSTRACT
Objective The CT values and glial fibrillary acidic Drotein (GFAP) expression changes within 24 hours in the cerebral infarction of rats were observed in order to evaluate the time of infarction indirectly. Methods The animal models of cerebral infarction due to the embolism of middle cerebral arteries were replicated reference to Longa’s thread embolism method. The rats with cerebral infarction in right hemisphere and without cerebral infarction in left cerebral hemisphere were scanned with CT at different time after cerebral infarction,then the CT values were measured and their differences were calculated. At the same time,the GFAP expression changes were detected by immunohistochemical technique (SP method). Results The infarction focuses were observed in all rats in 6 hours group. The differences of the CT values in the infarction hemisphere (right side in brain) and non-infarction (left side in brain) hemisphere had in linear relationship,and the GFAP expression also related to the time of infarction to certain degree. Conclusion Cerebral infarction due to embolism of blood vessel could be diagnosed at least 6 hours after middle cerebral artery occlusion. The time of cerebral infarction could be inferred by the difference of CT values between the infarction and non-infarction hemispheres and the changes of GFAP expression.
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Objective To investigate the effects of ephedrine on glial fibrillary acidic protein (GFAP) expression after cerebral ischemia-reperfusion injury in rats.Methods Altogether 60 male SD rats were randomly divided into sham-operation group,natural recovery group and ephedrine treatment group.The unilateral ischemia-reperfusion models were induced by clue-blocked method.The expression level of GFAP around ischemic area was examined by immunohistochemical technique at weeks 1,2,3 and 4 after operation.Results GFAP expression began to increase at 1 w and stabilized at 3 w in ephedrine treatment group and natural recovery group.There was a significant increase of GFAP expression in ephedrine treatment group compared with that in natural recovery group (P