葛根素预处理对大鼠局灶性脑缺血-再灌注线粒体功能的影响

目的观察葛根素对大鼠局灶性脑缺血-再灌注损伤后线粒体功能的影响。方法健康成年雄性SD大鼠40只,随机分成5组(n=8):假手术组、脑缺血-再灌注组、葛根素预处理24h 100mg组、葛根素预处理24h 200mg组和葛根素预处理24h 400mg组,其中葛根素预处理24h组于脑缺血前24h给予相应剂量葛根素腹腔注射行单次预处理,采用大脑中动脉线栓法建立局灶性脑缺血-再灌注模型,缺血90min,再灌注24h后,测定缺血侧海马线粒体内游离MDA、SOD、Na+-K+-ATP酶及Ca2+-ATP酶活性。结果与脑缺血-再灌注组相比,葛根素预处理-24 h100mg组、葛根素预处理-24h 200mg组及葛根素预处理-24h 400mg组大鼠脑线粒体内MDA含量明显下降,SOD、Na+-K+-ATPase、Ca2+-ATPase活性明显升高(P<0.05),而在葛根素预处理3个剂量组间比较差异均无统计学意义(P﹥0.05)。结论葛根素预处理对脑缺血-再灌注后线粒体损伤具有非剂量依赖性保护作用。     

原花青素对大鼠脑缺血再灌注损伤代谢障碍的影响

目的 探讨原花青素(PC)对大鼠脑缺血再灌注损伤代谢障碍的影响.方法 采用Zea-Longa线栓法制备大鼠局灶性脑缺血再灌注模型.术前0.5 h和脑缺血2 h时给予大鼠PC溶液50、100、200 mg/kg,假手术组和模型组分别给予等量的生理盐水.观察不同剂量PC溶液对大鼠脑缺血再灌注后神经功能状态、脑组织含水量及乳酸含量、能量代谢酶(Na+-K+-ATP酶和Ca2+-ATP酶)活性的影响.结果 PC中、高剂量组神经功能行为学评分和脑组织含水量显著低于模型组(P＜0.05).PC低、中、高剂量组脑组织乳酸含量显著低于模型组(P＜0.05).PC中、高剂量组Na+-K+-ATPase活性较模型组升高(P＜0.05).PC高剂量组Ca2+-ATPase活性较模型组有所增高(P＜0.05).结论 PC可通过减轻脑水肿、改善脑组织的代谢障碍而发挥脑保护作用.     

桃仁红花煎剂对大鼠缺血再灌注后脑组织的保护作用

目的研究桃仁红花煎剂对大鼠局灶性脑缺血再灌注后脑组织的影响。方法 45只雄性SD大鼠随机平均为给药组、模型组和对照组。采用线栓法阻塞大鼠右侧大脑中动脉,使其缺血2h后再灌注24h建立局灶性脑缺血再灌注模型。术前2h和术后3、12h分3次灌胃给予桃仁红花煎剂,总剂量是40g/kg。通过神经行为评分评定大鼠神经功能变化,按干湿重法测定脑含水量,用氯化三苯基四氮唑法测定脑梗死范围,分光光度法测定缺血区脑组织中Na+-K+-ATP酶和Ca2+-ATP酶的活性。结果在缺血再灌注3h和24h后,给药组神经行为评分明显高于模型组(P<0.05)。缺血再灌注24h,给药组脑含水量和脑梗死体积明显少于模型组(P<0.05);给药组缺血脑皮层中Na+-K+-ATP酶和Ca2+-ATP酶活性明显高于模型组(P<0.05)。结论桃仁红花煎剂对大鼠缺血再灌注后脑组织有保护作用,其机制可能与其增强Na+-K+-ATP酶和Ca2+-ATP酶的活性、减轻脑水肿有关。     

肢体缺血后处理对糖尿病大鼠脑缺血再灌注损伤线粒体结构和功能的影响

目的探讨肢体缺血后处理(I-PostC)诱导的远隔器官I-PostC(RPostC)对糖尿病大鼠局灶性脑缺血再灌注(I/R)损伤线粒体结构和功能的影响。方法链脲佐菌素空腹腹腔注射制作糖尿病大鼠模型,线栓法闭塞大脑中动脉(MCAO)制作局灶性I/R大鼠模型。造模成功的40只雄性SD大鼠分为4组:空白对照组、假手术组、I/R组,RPostC组,每组10只。I/R6h后取脑组织行HE染色观察,测定线粒体丙二醛(MDA)含量、超氧化物歧化酶(SOD)、Na+/K+-ATP酶、Ca2+-ATP酶和谷胱甘肽过氧化物酶(GSH-Px)活性,观察线粒体超微结构的改变。结果I/R组线粒体MDA含量[(4.99±1.25)nmol/mgprot]较空白对照组和假手术组明显升高(均P<0.01),SOD[(72.52±13.07)U/mg]、Na+/K+-ATP酶[(3.17±0.34)μmolPi/(mg.h)]、Ca2+-ATP酶[(1.56±0.23)μmolPi/(mg.h)]和GSH-Px活性[(22.66±5.29)U/mg)]明显降低(均P<0.01);与I/R组比较,RPostC组MDA含量[(3.58±0.91)...     

缺血后处理对糖尿病大鼠局灶性脑缺血再灌注损伤线粒体的影响

目的观察缺血后处理(I-Post)对糖尿病大鼠局灶性脑缺血再灌注损伤线粒体超微结构和功能的影响,探讨I-Post诱导的脑保护的可能机制。方法采用链脲佐菌(STZ)腹腔注射建立糖尿病大鼠模型,在此基础上通过线栓法建立大鼠大脑中动脉阻塞/再灌注模型。SD糖尿病大鼠随机分为4组(n=10),空白对照组、假手术组、缺血再灌注组(I/R组)、缺血后处理组(I-Post组)。于缺血90min再灌注6h后电镜下观察线粒体超微结构、测定缺血侧脑组织线粒体中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、Na+/K+-ATPase和Ca2+-ATPase活性。结果缺血后处理能明显减轻I/R引起的线粒体超微结构的损伤,提高线粒体SOD、GSH-Px、Na+/K+-ATPase和Ca2+-ATPase的活性(P<0.05或0.0),降低MDA的含量(P<0.05)。结论线粒体可能在I-Post诱导的脑保护中起关键性作用,I-Post诱导的脑保护机制可能与SOD、Na+/K+-ATP酶、Ca2+-ATP酶和GSH-Px活性增加有关。     

促红细胞生成素在脑缺血再灌注损伤中对线粒体的保护作用

目的 探讨促红细胞生成素(EPO)在脑缺血再灌注损伤中对线粒体功能的保护作用. 方法 30只SD大鼠按随机数字表法分为正常对照组、缺血再灌注组和EPO治疗组3组,每组各10只.EPO治疗组和缺血再灌注组用线栓法复制脑缺血再灌注模型.EPO治疗组在缺血再灌注后1、24、48、60 h腹腔注射EPO,剂量为3000 U/kg(用生理盐水以1:1比例稀释),缺血再灌注组腹腔注射同等剂量的生理盐水.正常对照组仅分离颈部动脉,动脉不做栓塞处理.缺血后72h观察各组大鼠脑组织神经细胞线粒体跨膜电位、线粒体丙二醛、超氧化物歧化酶、Na十_K+.ATP酶活性、一氧化氮含量和免疫组化检测海马区Caspase-3阳性细胞数的变化. 结果 EPO治疗组的神经细胞线粒体跨膜电位(77.48±5.93)、超氧化物歧化酶[(96.91±8.66)p,kat/g]、Na+_K+-ATP酶活性[(10.48±2.77)μkat/g]明显高于缺血再灌注组[44.47±17.35、(84.46±8.54)μkat/g、(7.37±2.87)μkat/g],线粒体丙二醛[(37.99±5.38)μmol/g]、一氧化氮含量[(10.18±2.02)μmol/g]、Caspase-3阳性细胞数(66.31±8.09)明显低于缺血再灌注组[(44.83±6.48)μmol/g、(12.12±2.14)μmol/g、74.90±7.42]. 结论 EPO对缺血再灌注损伤脑组织产生保护作用的重要机制之一是保护神经细胞线粒体的功能,其核心是抑制线粒体跨膜电位的下降.     

maFGF对慢性衰老大鼠脑组织中ATP酶活力的影响

目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力的影响,探讨maFGF抗衰老的机制。方法选择成年Wistar大鼠40只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老对照组、NS对照组和maFGF治疗组。另10只不注射D-半乳糖作为正常对照组。maFGF治疗组按12μg/kg剂量肌内注射,1次/d,共14 d,NS对照组肌肉注射与maFGF治疗组相同容量的生理盐水,1次/d;衰老对照组不作任何干预。各组大鼠到相对应的时间点取出各组大鼠脑组织,测定脑组织匀浆中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力。结果与正常对照组相比,衰老对照组大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力均明显著降低(P<0.01);maFGF治疗组脑组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于衰老对照组、NS对照组(P<0.05)。结论 maFGF能升高衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,对衰老大鼠脑损伤有一定保护作用。     

异丙酚预处理对大鼠脑缺血再灌注损伤早期中性粒细胞弹性蛋白酶活性及炎性因子表达的影响

目的 探讨异丙酚预处理对大鼠脑缺血再灌注(IR)损伤早期中性粒细胞弹性蛋白酶(NE)活性及炎性因子肿瘤坏死因子(TNF)-α和白介素(IL)-1β表达的影响.方法 健康雄性SD大鼠50只,随机分为正常对照组(NC组)、IR组、异丙酚低剂量组(P1组,50 mg/kg)、中剂量组(P2组,100 mg/kg)和高剂量组(P3组,150 mg/kg).采用线栓法建立大鼠大脑中动脉局灶性IR损伤模型.各异丙酚组分别于脑缺血前10min经腹腔注射相应剂量的异丙酚.大鼠脑缺血2h、再灌注24h给予神经功能缺损评分,采用酶联免疫吸附法检测脑组织NE活性及TNF-α和IL-1β的表达.结果 各异丙酚组神经功能缺损评分明显低于IR组(均P＜0.01);与NC组比较,IR组和各异丙酚组脑组织NE活性及TNF-α、IL-1β表达明显升高(均P＜0.01);与IR组比较,各异丙酚组NE活性及TNF-α、IL-1β表达明显降低(均P＜0.01);P2组NE活性及TNF-α、IL-1β表达明显低于P1组和P3组(均P＜0.01).结论 异丙酚预处理可抑制脑组织NE活化和TNF-α、IL-1β过度表达,降低炎性反应,对脑组织IR损伤早期具有保护作用;异丙酚100 mg/kg预处理的作用最佳.     

硫酸镁对大鼠急性脑缺血再灌注损伤时ATP酶的影响

目的　探讨镁剂在动物实验性急性脑缺血再灌注 (cerebral ischemia-reperfusion,CIR)过程中对 ATP酶的影响。方法　选用 Wistar大鼠 ,按改良的 Pulsinelli法建立了大鼠颈总动脉 CIR损伤模型 ;CIR损伤 1 5 min后 ,断髓处死鼠 ,取额叶脑组织测定 ATP酶含量。结果　急性 CIR早期 ,脑中 Na -K -ATP酶活性降低极显著(P <0 .0 1 ) ,Mg2 -ATP酶和 Ca2 -ATP酶活性降低显著 (P <0 .0 5 ) ;预先应用 Mg SO4 能稳定 ATP酶的活性(Mg2 -ATP酶 ,P <0 .0 1 ;Ca2 -ATP酶、Na -K -ATP酶 ,P <0 .0 5 )。结论　 Mg SO4 对大鼠 CIR损伤的脑保护作用与防止脑内多种 ATP酶活性降低有关。     

异丙酚介导的RhoA/ROCK2信号通路对脑缺血再灌注后神经炎症、细胞凋亡和脑梗死的作用

目的 探讨异丙酚对脑缺血再灌注大鼠神经炎症、细胞凋亡和脑梗死的作用与保护机制。方法 将30只SD大鼠随机分为假手术(Sham)组、脑缺血再灌注(I/R)组和异丙酚(Propofol)组,Sham组与I/R组使用水合氯醛(300 mg/kg)麻醉,异丙酚组应用异丙酚(60mg/kg)麻醉; 大脑中动脉闭塞造模2 h后恢复血供,24 h后进行神经功能缺损评分,取脑组织进行TTC染色、炎性细胞因子水平检测、免疫组化、Western blot实验。结果 I/R组大鼠神经功能受损,缺血侧梗死严重; Western Blot检测显示RhoA/ROCK2蛋白表达增加,Caspase-3蛋白剪切增加; 免疫组化显示Iba1激活,GFAP活化,即神经炎症反应增加。此外,Nissl小体减少,TUNEL阳性细胞数增加,即神经元凋亡增加; 异丙酚组RhoA/ROCK2蛋白表达水平、Caspase-3蛋白剪切显著降低,神经炎症反应减轻与神经元凋亡减少,神经功能缺损评分降低与脑梗死面积减少。结论 异丙酚可能通过抑制RhoA/ROCK2信号通路来减轻脑中神经炎症反应和减少神经元凋亡,从而改善神经功能与脑部梗死情况。     

改构型酸性成纤维细胞生长因子干预慢性衰老模型大鼠脑及肝组织和血液ATP酶的活力

背景：有研究表明改构型酸性成纤维细胞生长因子是多功能生长因子,但其抗衰老作用至今尚未有报道。 目的：观察改构型酸性成纤维细胞生长因子对D-半乳糖致衰老大鼠脑组织、肝组织及红细胞膜Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力的影响。 方法：将Wistar大鼠采用皮下注射D-半乳糖建立衰老模型,建模成功后随机分为模型组、生理盐水对照组和改构型酸性成纤维细胞生长因子组,另设正常对照组。改构型酸性成纤维细胞生长因子组按12 µg/kg剂量肌肉注射改构型酸性成纤维细胞生长因子,生理盐水对照组肌肉注射等量的生理盐水,模型组不干预。 结果与结论：与正常对照组相比,模型组大鼠脑组织、肝组织及红细胞膜Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显著降低(P < 0.01)。改构型酸性成纤维细胞生长因子组脑组织、肝组织及红细胞膜Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于模型组和生理盐水对照组(P < 0.05)。结果提示,改构型酸性成纤维细胞生长因子能提高衰老大鼠脑组织、肝组织及红细胞膜Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力,具有延缓衰老作用。     

Cromakalin pretreatment affects mitochondrial structure and function in a rat model of ischemia/reperfusion injury

BACKGROUND: Mitochondrial structural changes and energy dysmetabolism frequently occur subsequent to cerebral ischemia. Adenosine triphosphate (ATP)-sensitive potassium channel openers exhibit protective effects on cerebral ischemia/reperfusion injury. OBJECTIVE: To validate the effects of cromakalin on mitochondrial structure and function in ischemic penumbra brain tissue in a rat model of middle cerebral artery occlusion (MCAO). DESIGN, TIME AND SETTING: The present single-factor analysis of variance, randomized, controlled, animal experiment was performed at the Institute of Brain Science, Affiliated Hospital of Qingdao University Medical College between October 2007 and March 2008. MATERIALS: Forty male, Wistar rats were randomly divided into four groups, with 10 rats per group: sham-operated, MCAO, MCAO ATP-sensitive potassium channel opener (cromakalin), and MCAO eromakalin ATP-sensitive potassium channel blocking agent (glibenclamide). METHODS: Focal cerebral ischemia/reperfusion injury was induced by MCAO in all groups except the sham-operated group. The MCAO cromakalin group was administered 10 mg/kg cromakalin (i.p.) prior to MCAO induction. The MCAO cromakalin glibenclamide group received an injection of 10 mg/kg cromakalin (i.v.), and subsequently an injection of 10 mg/kg cromakalin (i.p.) prior to MCAO induction. MAIN OUTCOME MEASURES: At 24 hours after cerebral ischemia/reperfusion injury, cellular apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick-end labeling technique. Cytochrome C expression was measured by immunohistochemistry. In addition, mitochondrial swelling, membrane fluidity, membrane phospholipid and malonaldehyde (MDA) contents, as well as Na -K -ATPase, Ca2 -ATPase, and superoxide dismutase (SOD) activities were determined. RESULTS: Compared with the sham-operated group, the three ischemia groups exhibited significantly elevated mitochondrial MDA content, reduced membrane phospholipid and ATP contents, down-regulated membrane fluidity, and reduced Na -K -ATPase, Ca2 -ATPase, and SOD activities (P < 0.05-0.01 ). In the MCAO eromakalin group, the number of apoptotic cells decreased, and cytochrome C expression, as well as MDA content, were reduced. However, ATP content and Na -K -ATPase, Ca2 -ATPase, and SOD activities significantly increased compared with the MCAO group (P < 0.05-0.01 ). Glibenclamide noticeably antagonized cromakalin protection of mitochondria.CONCLUSION: Pretreatment with the ATP-sensitive potassium channel opener cromakalin increased mitochondrial Na -K -ATPase, Ca2 -ATPase, and SOD activities, decreased neuronal apoptosis, and inhibited cytochrome C expression following MCAO.     

丹参酮IIa拮抗脊髓缺血再灌注损伤：干预谷氨酸释放的上游因素

目的：探讨丹参酮调控谷氨酸转运体功能对脊髓缺血再灌注损伤的作用。方法：88只SD 大鼠结扎腹主动脉,制作脊髓缺血再灌注损伤模型。按随机数字表法将动物分为假手术组（n=8）,模型组（n=40）和丹参酮组（n=40）。分别在脊髓缺血再灌注损伤后0.5h、1h、4h、8h、12h相应时点检测各组谷氨酸转运体功能和Na+-K+−ATP酶活性。结果： ①大鼠脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性在脊髓缺血再灌注损伤后0.5h后开始下降,4h后降到最低点,其后活性逐渐恢复,但12h后仍未及正常水平。②丹参酮组各观测点脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性均较其它两组高。结论：①大鼠脊髓缺血再灌注损伤时脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性均下降;②丹参酮可能通过保护脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性的下降,从而减轻大鼠脊髓缺血再灌注损伤。     

Chlordecone toxicity: effect of withdrawal of treatment on ATPase inhibition

Adult male Sprague-Dawley rats were treated P.O with 10 mg/kg/day chlordecone for 10 days. Five rats from control group receiving corn oil and five rats from chlordecone group were sacrificed for tissue preparations. The remaining rats in chlordecone group were withdrawn from treatment and left in cages for 45 days. At 15, 30 and 45 days after withdrawal, 5 rats from each group with equal number of controls were sacrificed. Brain, liver and kidney were removed and subcellular fractions were prepared. Na+-K+, oligomycin-sensitive and oligomycin-insensitive Mg2+ ATPases were determined. Rats treated with chlordecone for 10 days showed a significant reduction of Na+-K+ ATPase activity in brain and kidney. The decreased enzyme activity in kidney but not in brain returned to normal within 15 days of treatment withdrawal. In brain the enzyme activity stayed at reduced level throughout the experimental period. Oligomycin-sensitive Mg2+ ATPase activity in all the tissues was decreased significantly in chlordecone treated rats. The enzyme activity returned to normal levels in all tissues gradually by 30 days of treatment withdrawal. Oligomycin-insensitive Mg2+ ATPase activity was not decreased in any tissue by chlordecone treatment. These results suggest that chlordecone effects on ATPase system are reversible except for Na+-K+ ATPase in brain.     

The effects of the pre-treatment of intravenous nimodipine on Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, lipid peroxidation and early ultrastructural findings following middle cerebral artery occlusion in the rat

Excessive calcium influx has been implicated in the pathophysiology of ischemic cerebral damage. The effects of nimodipine, a calcium antagonist, on the Na(+)-K+/MG+2 ATPase activity, Ca+2/Mg+2 ATPase, lipid peroxidation, and early ultrastructural findings were examined at the acute stage of ischemia in the rat brain. Ischemia was produced by permanent unilateral occlusion of the middle cerebral artery. In Group I, the rats which had no ischemia and not received medication were used for determining Na(+)-K+/Mg+2 ATPase, Ca+2/Mg+2 ATPase, the extent of lipid peroxidation by measuring the malondialdehyde content and normal ultrastructural findings. In Group II, the rats which had only subtemporal craniectomy without occlusion and received saline solution were used for determining the effect of the surgical procedure on the biochemical indices and ultrastructural findings. In Group III, the rats received saline solution following the occlusion in the same amount of nimodipine and in the same duration as used in Group IV. In Group IV, nimodipine pre-treatment 15 min before occlusion (microgram kg-1 min-1 over a 10 min period) was applied i.v. Na(+)-K+/Mg+2 ATPase and Ca+2/Mg+2 ATPase activities decreased significantly and promptly as early as 10 min and remained at a lower level than the contralateral hemisphere in the same group and at the normal level in Group I. Nimodipine pre-treatment immediately attenuated the inactivation of Na(+)-K+/Mg+2 ATPase (p < 0.05) but there was no change on Ca+2/Mg+2 ATPase activity (p < 0.05). Malondialdehyde content increased significantly in Group III following ischemia as early as 30 min. Nimodipine pre-treatment decreased the malondialdehyde level in Group IV (p < 0.05). This study supports the possibility that nimodipine pre-treatment effects the membrane stabilizing properties via inhibiting the lipid peroxidation and subsequently restoring some membrane bound and lipid dependent enzymes' activity such as Na(+)-K+/Mg+2 ATPase and the ultrastructural findings.     

Nicardipine reduces calcium accumulation and electrolyte derangements in regional cerebral ischemia in rats

We studied the effects of the calcium channel blocker nicardipine on regional tissue Ca2+, Na+, K+, and water shifts in the brains of seven Sprague-Dawley rats after permanent occlusions of the middle cerebral artery. We also assessed the entry of [14C]nicardipine into the brains of five rats; the highest concentrations of [14C]nicardipine were in the infarcted area. Nicardipine treatment significantly reduced Ca2+ accumulation in the middle cerebral artery territory by 60% compared with six untreated rats 6 hours after arterial occlusion. Eight 125-micrograms/kg boluses of nicardipine given every 30 minutes starting 5 minutes after arterial occlusion also significantly reduced the Na+ and K+ shifts in the middle cerebral artery territory by 40% and 50%, respectively, 6 hours after arterial occlusion. Nicardipine appears to reduce Ca2+ accumulation more than it reduces Na+ and water accumulation and K+ loss. Our results suggest that a calcium channel blocker can protect brain tissues in a model of focal cerebral infarction by directly reducing Ca2+ entry into ischemic cells.     

Effects of propofol on amino acid neurotransmitter levels and neuronal apoptosis in the hippocampus in a rat model of ischemia/reperfusion injury

BACKGROUND： Excitatory amino acids including glutamic acid and aspartic acid play a neurotrophic role during early development of the central nervous system but go on to promote toxic effects. Inhibitory amino acids include γ-aminobutyric acid and glycine. Changes in their concentration can reflect the degree of injury to brain tissue after cerebral infarction. OBJECTIVE： To investigate the effects of propofol on amino acid neurotransmitter levels and neuronal apoptosis in the hippocampus in a rat model of ischemia/reperfusion injury. DESIGN： Randomized controlled animal study. MATERIALS： Sixty male Wistar rats were randomly divided into a sham operation group, model group and propofol （50, 100 and 150 mg/kg） groups （n = 12）. METHODS： Global brain models of ischemia/reperfusion injury were established in the model group and the propofol groups. The vertebral artery and common carotid artery were merely isolated in the sham operation group. Ten minutes before ischemia, rats in the propofol groups were induced with an intraperitoneal injection of propofol （50, 100 or 150 mg/kg）; rats in the model and sham operation groups were induced with an intraperitoneal injection of saline （5 mL）. MAIN OUTCOME MEASURES： Content of amino acids, neuronal apoptotic index and density of apoptotic neurons in the hippocampal CA1 region. RESULTS： After a 10-minute ischemia / 60-minute reperfusion, the content of glutamic acid and aspartic acid was significantly decreased in the propofol （50, 100 and 150 mg/kg） groups compared with the model group （P 〈 0.05 or P 〈 0.01）; but the content of γ-aminobutyric acid was significantly increased in the propofol （100 and 150 mg/kg） groups （P 〈 0.05）. After a 72-hour reperfusion, the neuronal apoptotic index was significantly decreased in the propofol （50, 100 and 150 mg/kg） groups compared with the model group （P 〈 0.05 or P 〈 0.01 ）, and the decrease was remarkable in the propofol （100 and 150 mg/kg） groups. After a 72-hour