小剂量阿司匹林对脑缺血-再灌注损伤的保护作用及机制

目的:观察6 mg.kg-1阿司匹林对大鼠脑缺血-再灌注损伤的保护作用及机制。方法:线栓法制作局部脑缺血2 h、再灌24 h模型,观察6 mg.kg-1阿司匹林对脑损伤面积、正常锥体神经元密度、脑病理学改变及血前列环素(PGI2)/血栓素(TXA2)、脑组织髓化过氧化物酶(MPO)、丙二醛(MDA)、ATP含量、凋亡细胞数目及Bcl-2和Bax基因蛋白的影响。结果:6 mg.kg-1剂量阿司匹林明显缩小再灌注引起的脑损伤范围,改善脑病理形态,抑制再灌注引起的正常神经元的丢失和凋亡细胞数目,提高Bcl-2/Bax,提高血PGI2/TXA2。但对脑组织MPO、MDA及ATP无明显影响。结论:6 mg.kg-1阿司匹林对脑缺血-再灌注损伤有明显保护作用,其机制可能与提高PGI2/TXA2、抑制细胞凋亡及提高Bcl-2/Bax有关。

灯盏细辛药效物质基础3,5-二咖啡酰奎宁酸对大鼠局灶性脑缺血-再灌注损伤的保护作用

目的研究3,5-二咖啡酰奎宁酸对大鼠实验性局灶性脑缺血-再灌注损伤模型的保护作用。方法采用线栓法阻塞大鼠脑中动脉(MCAO)制备局灶性脑缺血-再灌注损伤模型,观察3,5-二咖啡酰奎宁酸对模型大鼠状态、神经行为学的影响,以及对脑梗死比率及血清中丙二醛(MDA)、总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、一氧化氮(NO)和一氧化氮合酶(NOs)的影响。结果 3,5-二咖啡酰奎宁酸剂9.13、18.25mg/kg时均能明显降低模型大鼠脑梗死的比率(P<0.05),降低血清中MDA水平(P<0.01),增强T-SOD、CAT、GSH-Px的活性(P<0.05)。结论 3,5-二咖啡酰奎宁酸对脑缺血-再灌注损伤有较好的保护作用,其作用机制可能与抗自由基生成有关。

PACAP对神经系统疾病保护作用的研究进展

垂体腺苷酸环化酶激活肽(pituitary adenylate cyclase-activating polypeptide,PACAP)存在于中枢神经系统内,作为神经递质、神经调质、神经营养因子及生长因子通过多种途径发挥神经保护作用。对脑缺血-再灌注损伤、创伤性脑损伤、精神分裂症、焦虑症、帕金森病、阿尔茨海默病等重大疾病具有重要的神经保护作用。本文就PACAP对神经系统疾病的保护作用及其机制的研究进行综述。

Protective Effects of Tea Polyphenol on Cerebral Ischemia-Reperfusion Injury in Rats and Its Scavenging Oxy-radical and Anticerebral Lipid Peroxidation Effects

AIM To study the protective effects of tea polyphenol (TP) on cerebral ischemia reperfusion injury in rats and its scavenging oxygen free radical(OFR) activities and antilipid peroxidation in vitro . METHODS Cerebral ischemia reperfusion injury was produced by bilateral ligation of the common carotid arteries with vagus nerves and reperfusion for 45 min. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. Superoxide anion (O 2) from xanthine xanthine oxidase system and hydroxyl radical (·OH) from Fe 2+ -H 2O 2 system were determined with spectrophotometry. RESULTS During Cerebral ischemia reperfusion,TP improved the activities of superoxide dismutase ( P 【0 05), GSH peroxidase( P 【0 01) and catalase( P 【0 01), while decreasing the maiondialdchyde content in the brain( P 【0 05) and brain water content ( P 【0 01). Tea polyphenol possessed significantly scavenging effects on ·OH produced by Fenton reaction and O 2 produced by xanthine xanthine oxidase system (the IC 50 were 2 2 mmol·L -1 and 1 9 mmol·L -1 respectively). Tea polyphenol could significant inhibit the lipid peroxidation of cerbral mitochondrial membrane induced by ·OH in a concentration dependent manner. CONCLUSION The results indicate that tea polyphenol could protect the injury on cerebral ischemia reperfusion in rats for OFR, these effects may be related to its scavenging effects on oxygen free radicals and antilipid peroxidant.

EFFECTS OF ELECTROACUPUNCTURE ON EXPRESSION OF INTERCELLULAR ADHESION MOLECULE-1 IN THE RAT OF LOCAL CEREBRAL ISCHEMIA-REPERFUSION

Objective To investigate effects of electroacupuncture （EA） on expression of intercellular adhesion molecule-1 （ICAM-1） in the rat of local cerebral ischemia-reperfusion. Methods Eighty SD rats were randomly divided into a normal control group, a sham operation group, a model group and an EA treatment group, 20 rats in each group. The thread-obstruction method was used for preparation of ischemia-reperfusion model. Zea-Longa rating criteria were used for evaluation of nervous function disorder; Immunohistochemical SABC method was used for detection of ICAM-1 expression in the microvascular endothelial cell of the ischemic brain region, and ELISA method for the soluble ICAM-1 （slCAM-1） content in peripheral blood. Re. suits After cerebral ischemia-reperfusion, both ICAM-1 expression level in the microvascular endethelium cell of the ischemic brain region and slCAM-1 content in the peripheral blood significantly increased in the model group as compared with the normal group and the sham operation group （P〈0.01）; After EA treatment, the ICAM-1 expression level in the microvascular endothelial cell of the ischemic brain region and slCAM-1 content in the peripheral blood were significantly down-regulated in the EA treatment group as com- pared with the model group （P〈 0.05）. Conclusion After cerebral ischemia-reperfusion, the microvascular endothelial cell of the ischemic brain region releases ICAM-1, which induces inflammatory injury of cerebral tissues; EA treatment can decease the expression of ICAM-1, so as to prevent the brain from the injury.

The effects of Shuxuetong on the pathology of cerebral ischemia-reperfusion injury and GABA and TNF-α expression in gerbil models

Objective To study the protective effect and mechanism of Shuxuetong on gerbil brain tissue from the area of ischemia-reperfusion. Methods Cerebral ischemia-reperfusion animal model by transient clipping bilateral common carotid arteries in gerbils. Pathological changes in the hippocampal tissue were observed at different reperfusion time （12 h, 3 d, 7 d）. The expression levels of GABA and TNF-α in the hippocampal CA1 subfield were observed using immunohistochemitry at 12 h, 3 d after reperfusion. The difference of above indices among false operation group, ischemia-reperfusion group and treatment group were compared. Results The injuries of pathology to hippocampal area in ischemia-reperfusion group were more serious than treatment group. The expression levels of GABA in treatment group were significantly increased compared with ischemia-reperfusion group, but the expression levels of TNF-α between the two groups have no difference. Conclusion Shuxuetong has protective effect on brain tissue of ischemia-reperfusion by enhancing the expression of GABA in the hippocampal tissue.

ARGININE VASOPRESSIN GENE EXPRESSION IN SUPRAOPTIC NUCLEUS AND PARAVENTRICULAR NUCLEUS OF HYPOTHALAMOUS FOLLOWING CEREBRAL ISCHEMIA AND REPERFUSION

Background. Our previous studies indicated that the increased arginine vasopressin(AVP) in ischemic brain regions of gerbils could exacerbate the ischemic brain edema. This experiments is further clarify the relation between AVP and cerebral ischemia at the molecular level. Methods. The contents of AVP, AVP mRNA, AVP immunoreactive(ir) neurons in supraoptic nucleus(SON) and paraventricular nucleus(PVN) after cerebral ischemia and reperfusion were respectively determined by radioimmunoassay(RIA), immunocytochemistry(ⅡC), situ hybridization and computed image pattern analysis. Results. The contents of AVP in SON, PVN were increased, and the AVP ir positive neurons in SON and PVN were also significantly increased as compared with the controls after ischemia and reperfusion. And there were very light staining of AVP ir positive neurons in the other brain areas such as suprachiasmatic nucleus (SC) and periventricular hypothalamic nucleus (PE), but these have no significant changes as compared with the controls. During different periods of cerebral ischemia (30～120 min) and reperfusion (30 min), AVP mRNA expression in SON and PVN were more markedly increased than the controls. Conclusions. The transcription of AVP gene elevated, then promoting synthesis and release of AVP in SON, PVN. Under the specific condition of cerebral ischemia and reperfusion, the activity and contents of central AVP increased abnormally is one of the important factors which causes ischemia brain damage.

CHANGES OF MONOAMINES, PURINES AND AMINO ACIDS IN RAT STRIATUM AS MEASURED BY INTERCEREBRAL MICRODIALYSIS DURING ISCHEMIA/REPERFUSION

The aim of this study was to determine the time course of changes in extracellular fluid (ECF) concentrations of purines, amino acids, monoamines, and their metabolites in the striatum of rats during ischemia and reperfusion, using intracerebral microdialysis as the sampling technique. In rats subjected to 20 min forebrain ischemia by four-vessel occlusion, the concentrations of adenosine (Ade), inosine (Ino) and hypoxanthine (Hyp) were found to rise markedly. These changes were accompanied by dramatically elevated levels of aspartate (Asp), glutamate (Glu), taurine (Tau), γ-aminobutyric acid (GABA), dopamine (DA) and norepinephrine (NE), all of which gradually returned to baseline following reperfusion. Concomitantly, the levels of metabolite 3, 4-dihydroxyphenylacetic acid (DOPAC) . homovanillic acid (HVA), 5-hydroxyindole-3-acetic acid (5-HIAA) and xanthine (Xan) decreased during ischemia and gradually recovered 60～ 90 min after reperfusion. It was concluded that during global brain ischemia, the ECF is flooded with both potentially harmful (e. g. Asp, Glu, DA) and protective (e. g. Tau, GABA, Ade) agents.

Single-strand DNA damages and its relationship with morphological change of neurons at early stage of rat cerebral ischemia/reperf usion

Objective：To discuss the DNA-strand breaks at early stage of middle cerebral artery occlusion/reperfusion (MCAO/R). Methods: Neurons number and morphologic change were observed by Nissl stain method, and DNA strand breaks were in situ detected by using DNA polymerase- I Klenow fragment-mediat-ed nick end-labelling method (Klenow method). Results: Six hours after reperfusion, a few neurons in dam-aged regions appeared morphologic changes while a few Klenow-positive cells were detected (P<0. 01). Twenty-four hours after reperfusion lots of neurons showed morphologic change while the number of Klenow-positive cells immediately and remarkably increased (P<0. 01). Seventy-two hours after reperfusion the number of neurons decreased significantly and the number of Klenow-positive cells was also less than that in 24 h (P<0. 05). Conclusion: ① 24 h after reperfusion when the number of Klenow-positive cells reached peak value, DNA single-strand breaks (SSBs) took place in many Klenow-positive cells, and presumed that DNA SSBs might be an important step in DNA-damage procession which might be induced by free radicals. ② At the same time when lots of DNA SSBs were produced, many neurons in the damaged regions showed morphological change, which indicated that lots of neurons had already progressed to irreversible damages when DNA SSBs took place.

Effects of electroacupuncture at Fengchi(GB20)on motor function and GFAP/NeuN expression around the ischemic tissue of the motor cortex in MCAO rats

Objective:To investigate the potential mechanism of electroacupuncture(EA)at bilateral Fengchi(GB20)in treating cerebral ischemia-reperfusion injury and to provide a scientific basis for future experimental research and clinical applications.Methods:Forty male specific-pathogen-free Sprague-Dawley rats were randomly divided into four groups:a normal group,a normal with EA group,a model group,and a model with EA group,with 10 rats in each group.The normal group received no intervention.The normal with EA group received EA at bilateral Fengchi(GB20).The model group underwent middle cerebral artery occlusion(MCAO)using the suture.The model with EA group underwent MCAO and received EA at bilateral Fengchi(GB20).Cerebral blood flow was monitored using a laser Doppler cerebral blood flow meter.Neurologic damage was assessed using the neurologic deficit score,and motor ability was observed using the CatWalk gait system.The expression of glial fibrillary acidic protein(GFAP)and neuronal nuclei(NeuN)protein,the neuron markers,was detected by Western blotting.The protein expression levels of GFAP and NeuN,as well as the number of positive cells in the motor cortex,were detected using immunofluorescence.Results:Compared to the normal group,the cerebral blood flow values in the model group and the model with EA group decreased by more than 50%during the modeling process(P<0.01)and returned to pre-modeling levels after reperfusion(P>0.05).The neurologic deficit score increased(P<0.05),the average motor velocity decreased(P<0.05),GFAP protein expression and the number of positive cells in the motor cortex increased(P<0.05),and the NeuN protein expression and the number of positive cells decreased(P<0.05)in the model group.Compared to the model group,the neurologic deficit score decreased(P<0.05),the average motor velocity accelerated(P<0.05),GFAP and NeuN protein expression and the number of positive cells in the motor cortex increased(P<0.01)in the model with EA group.Conclusion:EA at bilateral Fengchi(GB20)can reduce neuronal loss and increase GFAP and NeuN protein expression in the motor cortex of rats after ischemia-reperfusion,improve the motor function after ischemic stroke,and accelerate the recovery of balance and stability of the affected limbs.

Relationship between transmembrane signal transduction pathway and DNA repair and the mechanism after global cerebral ischemia-reperfusion in rats

Objective To !nvestigate the protein levels of phospho-ERK and phospho-APE/Ref-1 in hippocampal neurons after global cerebral ischemia reperfusion in rats, and observe the relationship between transmembrane signal transduction and repair of DNA damage. The role of ERK signal transduction pathway following global cerebral ischemia reperfusion in rats is further discussed. Methods Ninety healthy male SD rats were divided into 3 groups randomly： Sham group （S group）, Ischemia reperfusion group （IR group） and Pd98059 pretreatment/ischemia reperfusion group （PD group）. Global cerebral ischemia reperfusion model was established by four-vessel occlusion （4-VO） method, and reperfusion was performed 5 minutes following ischemia. Protein levels of phospho-ERK and phospho-APE/Ref-1 were detected using immunohistochemical method at 2 h, 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion, and neuron apoptosis was observed by HE and TUNEL staining. Results In CA1 region of IR group, TUNEL positive cells began to appear at 6 h after IR, and reached the apex during 24 h to 48 h. However, TUNEL positive was most strongly exhibited in PD group. In IR group, phospho-ERK was obviously detected in CA3 region at 2 h after IR, and its level was phospho-ERK expression in PD group was weaker than gradually decreased from 6 h until totally absent at 48 h. Besides, that in IR group. For phospho-APE/Ref-1, its expression began to appear in CA1 region in IR group at 2 h after IR, with no obvious changes during 2 h to 12 h. Phospho-APE/Ref-1 expression began to decrease at 24 h and this decrease continued thereafter. Expression level of phospho-APE/Ref-1 in PD group was lower than that in IR group. Results showed the concurrence of decreased phospho-ERK expression level and increased neuron apoptosis after cerebral ischemia reperfusion, the former of which was consistent with the decrease of phospho-APE/ Ref- 1 expression. Also, the greater the inhibition of ERK phosphorylation was, the greater decrease of APE/Ref- 1 expression occurred. Conclusion Activation of ERK signal transduction pathway increased the expression of phospho-APE/Ref-1, and thus faciliated the repair of DNA damage. So, activation of ERK signal transduction pathway may protect neurons from apoptosis after cerebral ischemia reperfusion.

Management of cerebral ischemia due to Takayasu's arteritis

OBJECTIVE: To explore the management of cerebral ischemia caused by Takayasu's arteritis. METHODS: Ninety-three cases treated from June 1984 to September 1999 at the General Post & Telecom Hospital, the Sir Run Run Shaw Hospital, the First Affiliated Hospital of Zhejiang University, the Second Medical College of Beijing University, Beijing An Zhen Hospital, and the Beijing Union Medical College Hospital, including 10 men and 83 women, were reviewed. Of the 93 cases, bypasses from the ascending aorta to the axillary or subclavian artery and from graft to the carotid artery were performed in 47 cases. Subclavian to carotid bypass was performed in six cases. Percutaneous transluminal angioplasty (PTA) was used in five cases and stenting in one. RESULTS: Marked improvement was achieved in 30.3%, fair in 34.9%, improvement in 21.2%, unchanged in 4.6%, and death in 9.0% before discharge; 30.6%, 38.8%, 16.3%, 4.1%, and 2.0% respectively during a mean follow-up of 48 months, and recurrence requiring revision in 8.2%. CONCLUSION: Patients with occlusive lesions of all four cervical arteries always have severe cerebral ischemia and their distal runoff is always unvisualised by angiography. However, we found by exploration that the internal carotid artery is patent in all but one patient. Therefore, an ascending aorta to carotid bypass is feasible in most instances, and this can and should be done when the cerebral perfusion is jeopardized at a time when the patient is in a stable or relatively stable condition. Unfortunately, the cerebral re-perfusion syndrome is still a serious and not completely solved problem.

Effects of eye-acupuncture on the expression of brainderived neurotrophic factor in the brain of rats with cerebral ischemia reperfusion

Objective To observe the effects of eye-acupuncture therapy and bodyacupuncture therapy on the expression of brain-deprived neurotrophic factor （BDNF） in rats with cerebral ischemia reperfusion injury （CIRI）. Methods According to random number table, 48 SD rats were randomly divided into 6 groups, including normal control group （group A）, sham operation group （group B）, model group （group C）, eye-acupuncture group （group D）, non-acupoint of eye-acupuncture group （group E） and body-acupuncture group （group F）, eight rats in each group. Artery infarction reperfusion model were prepared by using suture-occluded method. Liver region, upper energizer area, lower energizer area and kidney region were selected in the group D. Acupuncture was carried out at the point located at 3 mm from the acupoint areas in the group E. Qūchí （曲池 LI 11）, Zúsānl （足三里 ST 36） and other acupoints were selected in the group F. Zea Longa scoring method was utilized for scoring the neural functions of rats; real-time PCR was carried out to examine the expression level of BDNF mRNA in the brain 72 h after ischemia reperfusion; western blot was carried out to examine the expression level of BDNF protein in the brain 72 h after ischemia reperfusion. Results The symptoms of neurologic impairments in the rats of the group D were alleviated in comparison to those in the group C （P0.01）, and the difference between the group D and the group F was not statistically significant （P0.05）; Compared with the group C, the mRNA and protein expression levels of BDNF in the brain of rats in the group D and the group F both increased （P0.01）, but the difference between the group D and the group F was not statistically significant （P0.05）. Conclusion The functions of eye-acupuncture and body-acupuncture in improving cerebral ischemia reperfusion injury are similar, and the functional mechanisms for the two different therapies may be related to the up-regulation of BDNF expression in brain and thus promote the repairing of brain tissues.

Effect of electroacupuncture at Neiguan(PC 6) and Baihui(GV 20) on CHOP and caspase-12 gene expressions in rats after ischemia-reperfusion injury

Objective： To investigate the effects of electroacupuncture （EA） at Neiguan （PC 6） and Baihui （GV 20） by observing the changes of CCAAT/enhancer-binding protein（C/EBP） homologous protein （CHOP） and caspase-12 gene expressions in rats after cerebral ischemia-reperfusion injury （IRI）, and explore whether the apoptosis pathway of endoplasmic reticulum stress （ERS） is involved in the protective mechanisms of EA. Methods： Sixty rats were randomly assigned to five groups （12 in each group）： a normal control group （group A）, a sham-operation group （group B）, an operation group （group C）, an Edaravone group （group D） and an EA group （group E）. The cerebral IRI rat model was induced by middle cerebral artery occlusion （MCAO） using intraluminal monofilament. 2,3,5-triphenyl tetrazolium chloride （TTC） staining was adopted in the measurement of cerebral infarction volume. Real-time polymerase chain reaction （RT-PCR） was used to determine the mRNA expressions of CHOP and caspase-12. Results： Compared with group A and group B, the volume of cerebral infarction and mRNA expressions of CHOP and caspase-12 in group C, group D and group E were increased, with statistical significances （P〈0.05 or P〈O.01）; compared with group C, the volume of cerebral infarction and mRNA expressions of CHOP and caspase-12 in group D and group E were decreased significantly （P〈0.05 or P〈0.01）; there were no significant differences between group D and group E in comparing the above items （P〉0.05）. Conclusion： EA at Neiguan （PC 6） and Baihui （GV 20） can effectively suppress the volume of cerebral infarction. Furthermore, the underlying mechanism of EA at Neiguan （PC 6） and Baihui （GV 20） is possibly related to the down-regulation of CHOP and caspase-12 mRNA expressions, so as to decrease cell apoptosis.

Electroacupuncture on serum interleukin level in rat models of cerebral ischemia-reperfusion injury

Objective： To observe the effect of electroacupuncture （EA） on serum interleukin （IL）-6, IL-8 and IL-10 in rat models of cerebral ischemia-reperfusion, and to discover the mechanism of EA in preventing and treating cerebral ischemia. 〈br〉 Methods：Male Sprague Dawley （SD） rats were randomized into a sham-operation （SO） group, a model control （MC） group, and an EA group, which were sub-grouped into a 6-hour group and a 24-hour group. In the SO group, rats only received vessel separation with filament placed inside without any treatment. In the MC and EA groups, the focal cerebral ischemia-reperfusion model was induced by using modified Longa method with intraluminal filament. The MC group didn’t receive any treatment;the EA group received EA at Baihui （GV 20） and Dazhui （GV 14） with sparse-dense wave for 30 min. The levels of serum IL-6, IL-8 and IL-10 were detected by using Elisa test. 〈br〉 Results： Six hours after ischemia-reperfusion injury, the levels of serum IL-6, IL-8 and IL-10 in the MC group were significantly higher than those in the SO group （P〈0.01, P〈0.05, P〈0.05）;the level of serum IL-8 in the EA group was significantly lower than that in the MC group （P〈0.05）, while there were no significant differences in comparing IL-6 and IL-10 between the EA group and the MC group. Twenty-four hours after ischemia-reperfusion injury, the levels of serum IL-6 and IL-8 in the EA group were significantly lower than those in the MC group （both P〈0.05）, while there were no significant differences in comparing the level of IL-10 among the three groups. 〈br〉 Conclusion：Early intervention by EA can regulate the levels of serum IL-6 and IL-8 in cerebral ischemic injury.

The proteomic study and the target discovery of W026B, a new compound with brain protective effect

W026B is a new compound that has a protective effect on cerebral ischemia reperfusion(I-R)injury in mice,while its specific mechanism is still unknown.In this study,proteomics was used to observe the effect of W026B on protein expression in brain I-R tissue,and to reveal its potential target.A total of 42 significantly altered proteins were identified in both brain I-R model and W026B treatment from 4852 proteins detected by proteomics,and most of these proteins were related to immunity and inflammation,metabolism,neuroprotection as well as cell proliferation and cell structure.Western blotting analysis showed that three out of five selected proteins showed consistent alteration with the proteomics.Regulator of G protein signaling 17(RGS17)was selected for further study,and its knockdown by siRNA RGS17 aggravated brain injury and abolished the protective effect of W026B.W026B could bind with RGS17(KD:6.04×10–6 mol/L).The knockdown of RGS17 aggravated Neuro-2 a cell damage induced by group I metabotropic glutamate receptors(mGluRs)agonist,and abolished the protective effect of W026B.In conclusion,W026B protected brain against I-R injury by affecting diverse proteins.RGS17 might be one of its targets and a potential therapeutic target of brain I-R injury.The upstream receptor of G protein,which was regulated by RGS17 and affected by W026B,might be group I m GluRs.This study provided useful evidence for the further R&D and the potential clinical application of W026B.

Effects of Electroacupuncture on the Ability of Learning and Memory in Rats with Ischemia-reperfusion Injury

Objective： To observe the effects of pretreatment and treatment with electroacupuncture on the ability of learning and memory in rats with ischemia-reperfusion injury, and to provide the research basis for preventing and treating the disorder of learning and memory in patients with apoplectic sequelae. Methods： Seventy-two SD rats, clean class, were randomly divided into sham operation group, model group, pretreatment group, and treatment group. The step-through latency and number of errors, nerve injury score, and the number of cholinoceptor in the affected hippocampus were recorded to analyze the effects of pretreatment and treatment with electroacupuncture on the ability of learning and memory in rats with ischemia-reperfusion injury. Results： 1） The rats with ischemia had various signs of nerve injury. Compared with that in the sham operation rats, the nerve injury score in the model rats was lower, the step-through latency and number of errors were increased, and the content of special mAchR was decreased （P〈0.05）; 2） Electroacupuncture could decrease the nerve injury score of the model rats. Compared with those in the model group, the step-through latency and number of errors all had significant difference in the pretreatment and treatment groups （P〈0.05）; 3） Compared with that in the model group, the content of mAchR was increased in the pretreatment group （P〈0.05）, and increased a little in the treatment group. Conclusion： Pretreatment and treatment with electroacupuncture can prolong step-through latency, and

Dynamic Changes of Glycine and Taurine in Corpus Striatum of Rats with Ischemia-reperfusion Injury and Effects of Electroacupuncture

Objective： To investigate the dynamic changes of glycine （Gly） and taurine （Tau） in corpus striatum of rats with ischemia-reperfusion injury （IRI）, and the regulation effect of electroacupuncture on them. Methods： Thirty SD rats were randomly divided into sham surgery group, model group, and treatment group. Rats in the sham surgery group were operated without ischemia. Rats in the model group and treatment group were operated to make model of cerebral IRI. The ischemia status lasts 1.5 h, and reperfusion was performed for 3.75 h. Rats in the treatment group were treated with electroacupuncture at Fengchi （GB 20）. Neurologic deficit score （NDS） was used to evaluate the rats functions. Microdialysis and High Performance Liquid Chromatography technique were used to detect the changes of Gly and Tan in corpus striatum of rats. Results： Contents of Gly and Tan increased at 1.5 h after ischemia. Them decreased to level as same as those rats in the sham surgery group after reperfusion. The content of Gly in the model and treatment group increased again at 2-2.5 h after reperfusion, and then decreased to the same level of the sham surgery group. There was a third increase of Gly content in the treatment group at 2.75 h after reperfusion. Electroacupuncture treatment could delay the decrease of Tan content after reperfusion, and make it increase at 1.5, 2 and 2.75 h after reperfusion. The peak appeared in the last time. NDS in the model and treatment group were more than that in the sham surgery group, and lowered at 5.25 h after surgery. Effects in treatment group was better than that in the model group （P〈0.05）. Conclusion： IRI makes contents of Gly and Tau in corpus striatum increase at a special time. Electroacuptmcture treatment could increase contents of Gly and Tau at a special time after reperfusion, which maybe an important mechanism of protecting effects of electroacupuncture on the brain.

Effects of Electroacupuncture plus Dopamine D1 Receptor Antagonist on Somatosensory Evoked Potentials and Behavioral Changes in Rats with Cerebral Ischemia-reperfusion

Objective： To explore the effects of electroacupuncture （EA） plus dopamine D 1 receptor （D 1 R） antagonist on somatosensory evoked potentials （SEP） and behavioral changes in rats with cerebral ischemia- reperfusion. Methods： Forty rats were randomly divided into a normal group, a model group, an EA group, a D1R antagonist group and an EA＋D1R antagonist group, with 8 rats in each group. Ischemia-reperfusion model was established in the other 4 groups except the normal group, and they were treated by different ways after modeling successfully. SEP, neural function defect score （NFDS） and beam walking tests were performed before and after modeling, before sacrifice respectively. Results： SEP of the EA group, D1R antagonist group and EA＋D1R antagonist group showed significant differences when compared with that of the model group （P〈0.05） after treatment. Before treatment, behavioral tests of the model group showed significant decreases compared with those of the normal group （P〈0.05）. After treatment, behavioral tests in the EA group, the D 1R antagonist group and the EA＋D 1R antagonist group improved obviously and showed statistical differences compared with those in the model group （P〈0.05）. Conclusion： EA and D1R antagonist treatments could both promote the neural functional recovery after ischemia-reperfusion and play a brain-protective role, but there was no synergistic effect of EA and D 1R antagonist in combination.