不同饲养环境对局灶性脑梗死大鼠梗死灶周围VEGF表达的影响

目的观察不同环境设置对局灶性脑梗死大鼠行为学恢复及梗死灶周围血管内皮生长因子(VEGF)表达的影响,为临床应用tr 6234丰富环境、探索学习等不同环境进行脑卒中康复治疗提供基础理论支持和实验依据。方法将实验动物随机分为假手术对照组(15只)和大脑中动脉阻塞(MCAO)组(90只)。手术组用电凝法造成右侧MCAO模型。MCAO组大鼠于MCAO手术后,再随机分为社会交往组(30只)、探索学习组(30只)、和丰富环境组(30只)。社会交往组5只一组,群居于标准笼;探索学习组10只一组,居于迷宫笼;丰富环境组30只居于丰富环境笼。MCAO各组分别于术后1d、3d、7d、14d、28d随机选取5只,假手术组于术后1d、3d、7d随机选取5只大鼠处死,剖颅取脑,石蜡包埋,切片,免疫组化染色,测定VEGF在脑梗死灶周围皮质的表达情况。结果 VEGF的表达,社交组MCAO术后1d可见梗死灶周围VEGF略有表达,3d表达略有增加(P<0.05)。MCAO各组可见术后第2w时表达增高明显,且均高于假手术组,(P<0.05)。随时间推移,至MCAO后28d时,丰富环境组、探索学习组及社会交往组VEGF表达略有下降。在14d时,丰富环境显著高于探索学习及社会交往组(P<0.05)。结论丰富环境、探索学习可上调局灶性脑梗死后大鼠梗死灶周围皮层VEGF的表达,这种上调可能是丰富环境、探索学习促进大鼠行为学功能恢复原因。     

社会交往对大鼠局灶性脑梗死灶周围SYN表达的影响

目的观察社会交往环境对局灶性脑梗死大鼠突触膜糖蛋白(Synaptophysin,SYN)表达的影响。方法SD大鼠75只。将实验动物随机分为假手术对照组(5只)和大脑中动脉阻塞组(MCAO)(70只)。MCAO组大鼠采用电凝法造成右侧大脑中动脉阻断(MCAO)模型后,再随机分为独居组(30只)、社会交往组(40只)。于不同时间点分批处死大鼠,用免疫组化染色观察梗死灶周围皮质SYN阳性表达。结果MCAO后梗死灶周围皮质SYN阳性表达均高于假手术对照组,并且随时间的推移,其表达进一步增高。社会交往组在1、2、3周SNY表达均明显优于独居组和对照组。结论社会交往能促进梗死灶周围SYN的表达。     

缺血后海马高迁移率族蛋白与星形胶质纤维酸蛋白表达及相关性

目的研究大鼠局灶性脑缺血再灌注星形胶质纤维酸蛋白(GFAP)与高迁移率族蛋白(HMGB1)在海马CA1区表达变化,探讨二者之间的关系。方法采用大脑中动脉栓塞2h制备SD大鼠脑缺血模型,60只雄性SD大鼠随机分为假手术组、缺血再灌注组,按1d、3d、7d、14d、28d时间点再分5个亚组,各时间点处死取脑,用免疫组化和荧光双标结合共聚焦扫描的方法来检测高迁移率族蛋白和星形胶质纤维酸蛋白在脑内海马CA1区表达变化。结果不同时间点缺血再灌注组GFAP、HMGB1表达均高于同时期的假手术组(P<0.05)。缺血再灌注组星形胶质细胞1d、3d、7d逐渐激活增生,7d达到高峰,14d开始下降;HMGB1在1d、3d、7d、14d是表达增加,14d达高峰,28d下降(与前一时间点比较P<0.05)。缺血再灌注组GFAP和HMGB1表达具有相关性(P<0.05),存在HMGB1和GFAP共定位细胞。结论脑缺血再灌注后,海马CA1区HMGB1增加与星形胶质细胞激活成正相关,过度表达的HMGB1和增殖的星形胶质细胞可能与缺血再灌注后神经元的迟发性损伤有关。     

电刺激治疗对脑梗死大鼠运动功能和脑组织微管相关蛋白-2及存活素表达的影响

目的探讨电刺激对脑梗死大鼠运动功能和脑组织微管相关蛋白-2(MAP-2)及存活素表达的影响。方法采用线栓法制作大鼠局灶性脑梗死模型。制模后24h起,分别给予大鼠瘫痪侧(单侧)或双侧肢体电刺激治疗3d、7d、14d和21d。电刺激前、后各时间点用平衡木试验(BWT)检测大鼠的肢体运动功能,用免疫组化染色检测梗死灶周围大脑皮质MAP-2和存活素的表达水平,并与脑梗死对照组和假手术组大鼠比较。结果治疗第7d起电刺激组大鼠瘫痪肢体的BWT评分明显高于对照组(均P<0.05),治疗14d起双侧电刺激组BWT评分明显高于单侧电刺激组(均P<0.05)。治疗第7d起,电刺激组梗死灶周围脑组织MAP-2表达水平明显高于对照组(均P<0.05);治疗14d起,双侧电刺激组MAP-2的表达水平明显高于单侧电刺激组(均P<0.05);治疗21d时与假手术组MAP-2表达水平比较差异无统计学意义。电刺激组治疗后各时间点梗死灶周围脑组织存活素表达水平明显高于假手术组(均P<0.05),治疗7d、14d存活素表达水平明显高于对照组(均P<0.05),达到高峰;而双侧电刺激组明显高于单侧电刺激组(均P<0.05);治疗21d时,电刺激组和...     

环维黄杨星D对高血压大鼠脑缺血神经胶质原纤维酸性蛋白与神经粘蛋白表达的影响

目的 观察中药单体环维黄杨星D（CVB-D）对易卒中型肾血管性高血压大鼠（RHRSP）脑缺血再灌注不同时间神经胶质原纤维酸性蛋白（GFAP）与神经粘蛋白（neurocan）表达的影响。方法 100只SD大鼠随机分成随机分为空白组10只（不作任何处理的RHRSP）、假手术组10只（仅作手术创伤分离动脉，不结扎动脉）、CVB-D治疗组40只、生理盐水对照组40只。采用环形银夹使SD大鼠的双侧肾动脉狭窄，制成RHRSP，再用线栓法制成一侧大脑中动脉闭塞（MCAO）模型。用免疫组化等方法观察CVB-D对脑缺血2h后再灌注1、7、14、30d不同时间点大鼠脑组织GFAP与neurocan表达。结果 缺血2h再灌注后．治疗组脑缺血区周围GFAP阳性表达细胞呈现先递增后减少的趋势。与对照组相比，除第1天外，第7、14、30天差异都有显著性意义（P〈0．05）。Neurocan在空白组、假手术组未见阳性细胞，缺血再灌注1d对照组出现neurocan阳性表达细胞，并且呈先递增后减少趋势。治疗组neurocan阳性表达细胞与对照组相比．除第1天外，第7、14、30天差异都有显著性意义（P〈0．05）。结论 CVB-D有促进RHRSP脑缺血损伤区神经功能的修复作用，可能与其下调神经抑制因子GFAP、neurocan的表达等机制密切相关。     

脂肪来源干细胞移植对脑缺血大鼠运动功能的影响

目的 观察脂肪来源干细胞(ADAS)移植入脑缺血大鼠后存活、迁移、分化以及大鼠的运动功能障碍恢复情况,探讨ADAS移植治疗大鼠局灶性脑缺血的有效性和可能机制. 方法 将雄性SD大鼠饲养至250～300 g时,制作左侧大脑中动脉阻塞模型(MCAO),按照随机数字表法分为未处理组、对照组和移植组,每组6只.未处理组造模后不作特殊处理,对照组在造模后3h通过尾静脉注射杜氏改良培养基(DMEM),移植组造模后3 h通过尾静脉注射ADAS.造模后14 d处死大鼠,通过免疫荧光染色观察5-溴脱氧尿嘧啶核苷(BrdU)、神经元特异性烯醇化酶(NSE)、人微管相关蛋白2(MAP-2)和神经胶质纤维酸性蛋白(GFAP)的表达.造模后1、7及14 d时神经功能缺损评分评价大鼠运动功能改善情况. 结果 (1)移植后,标记了BrdU的ADAS大量出现在缺血灶周围;(2)MCAO后14d,缺血灶周围出现了少量BrdU/GFAP双染阳性细胞;同时出现少量BrdU/NSE和BrdU/MAP-2双染阳性细胞;(3)14d时移植组大鼠神经功能缺损评分与对照组相比明显降低,差异有统计学意义(P＜0.05). 结论 (1)成年大鼠ADAS在MCAO大鼠体内存活并少量分化为神经元样细胞和星形胶质细胞样细胞;(2)移植ADAS可使大鼠脑缺血所致的运动功能缺损得到改善.     

Survivin和GFAP在大鼠脑出血后的表达及作用

目的 探讨生存素(Survivin)和胶质纤维酸性蛋白(GFAP)在大鼠脑出血后出血灶周围区的表达及作用.方法 健康雄性Wistar大鼠70只,随机分为实验组和对照组,实验组63只,采用白体血制作基底节脑出 血模型,分别在术后3h、12h、1d、2d、3d、5d、7d、14d和28d处死动物.对照组7只,采用相同方法注入等量生理盐水.HE染色观察组织病理变化,免疫组织化学方法检测Survivin和GFAP蛋白的表达,并对其进行定性和定量分析.结果 脑出血组:Survivin在12h即有明显增高,1d达高峰,2d后表达迅速下降,3d降至最低水平,至5d、7d表达义有升高,其增高与3d相比有统计学意义(P＜0.05)；GFAP的表达随出血时间的延长而增加,2d明显增高,7d达高峰.对照组:Survivin没有明显的表达；GFAP表达少量.结论 Survivin和GFAP在脑出血后出血灶周围区,以不同的方式参与损伤的修复.     

经颅磁刺激对脑梗死大鼠神经功能恢复及神经微丝蛋白表达的影响

目的研究经颅磁刺激(TMS)对脑梗死大鼠神经功能恢复和神经微丝蛋白(NFP)-200表达的影响。方法SD大鼠60只,采用线栓法制作脑缺血模型,随机分为TMS组与假刺激组(各30只),两组又分为1d、3d、7d、14d和21d组(每组6只)。TMS组大鼠给予TMS共200个脉冲,每天2次,按不同时间组持续相应天数。治疗后给两组大鼠进行神经功能缺损评分,采用免疫组化法检测梗死灶周围区域NFP-200的光密度值。结果治疗14d和21d时,TMS组的神经功能缺损评分(2.67±0.82,1.50±0.55)显著低于假刺激组(3.67±0.52,3.17±0.75)(P<0.05,P<0.01);TMS组大鼠脑梗死灶周围NFP-200的光密度值(1.363±0.045,1.581±0.037)显著高于假刺激组(1.290±0.026,1.473±0.037)(均P<0.01)。结论TMS可以促进脑梗死大鼠神经功能的恢复及脑梗死周围区域NFP-200表达上调。     

大鼠脑出血后活化星形胶质细胞EGFR-JAK1/STAT3表达及Genistein的抑制作用

目的探讨EGFR-JAK1/STAT3信号通路在大鼠脑出血后星形胶质细胞活化中的作用。方法 SD大鼠60只,随机分为ICH组、DMSO组、GST组,每组20只,Ⅶ型胶原酶注入苍白球进行脑出血造模。GST组在造模后每天腹腔注射Genistein溶液(50 mg/kg),DMSO组腹腔注射相同剂量DMSO溶液,一次/d。取术后1 d、7 d、14 d、28 d共4个时间点进行神经功能评分,各时间点每组随机取5只大鼠处死取脑,免疫组化检测EGFR、GFAP在星形胶质细胞中的表达变化,Western blot检测每各组p-JAK1、p-STAT3蛋白水平的表达。结果神经功能评分:GST组优于ICH组与DMSO组、ICH组与DMSO组比较差异无统计学意义(P>0.05);免疫组化显示脑出血后EGFR、GFAP表达增高,给予GST干预后,GFAP、EGFR表达显著少于ICH组及DMSO组,差异有统计学意义(P<0.05);7 d时p-JAK1/p-STAT3蛋白表达显著上升,予GST干预后,p-JAK1/p-STAT3蛋白水平较ICH组明显降低,差异有统计学意义(P<0.05),DMSO组EGFR、GFAP及p-JAK1/p-STAT3蛋白表达水平,与ICH组比较,差异无统计学意义(P<0.05)。结论脑出血所致星形胶质细胞活化与EGFR表达上调有关,抑制EGFR表达,可使pJAK1/p-STAT3蛋白表达水平下调,提示EGFR-JAK1/STAT3信号通路可能与脑出血后星形胶质细胞活化相关。     

经颅磁刺激对脑梗死大鼠神经功能恢复与皮层BDNF表达的影响

目的研究经颅磁刺激（transcranial magnetic stimulation，TMS）对脑梗死大鼠神经功能恢复和皮层脑源性神经营养因子（Brain derived neurotrophic factor，BDNF）表达的影响。方法成年健康雄性SD大鼠80只，随机分为脑梗死1、7、14、21、28d组及TMS1、7、14、21、28d组，每组各8只；采用线栓法制作左侧大脑中动脉闭塞的脑梗死模型；在规定的时间点行神经功能评定，应用免疫组化的方法检测梗死侧皮层BDNF的表达。结果（1）和脑梗死28d组相比，TMS28 d组大鼠Bederson神经功能评分、平衡木实验、网屏实验评分均较低，两者相比具有显著性差异（P〈0．01）；转棒实验虽评分较低，但2组无显著性差异（P〉0．05）；（2）大鼠脑梗死1d后梗死侧皮层可见较多BDNF阳性表达神经细胞，主要位于梗死灶周围，至第7d表达达高峰，然后开始下降；TMS7、14、21d组梗死侧皮层BDNF表达增加。结论TMS能促进脑梗死大鼠神经功能恢复，机理可能与TMS能增加脑梗死侧皮层BDNF表达有关。     

重复经颅磁刺激对脑梗死大鼠梗死侧皮质内源性神经干细胞激活、增殖的影响

目的研究重复经颅磁刺激(rTMS)对脑梗死大鼠神经功能恢复及梗死侧皮质内源性神经干细胞激活、增殖的影响。方法将72只雄性SD大鼠随机分为模型组、假刺激组、rTMS组,每组24只,各组根据脑梗死后不同时间点再分为1、7、14、21 d四个亚组,每个亚组6只。采用线栓法制作左侧大脑中动脉闭塞脑梗死模型。rTMS组于动物清醒后当天即给予每天2次、每次30个脉冲的rTMS治疗(频率为0.5 Hz,场强为1.33 T);假刺激组模拟rTMS固定大鼠头部放置线圈但不给予脉冲磁刺激;模型组不给任何治疗。各组在规定的时间点应用改良的神经功能缺损评分(mNSS)进行神经功能评定,治疗结束前24 h腹腔注射5-溴脱氧尿嘧啶核苷(BrdU),应用免疫组织化学技术检测梗死侧皮质巢蛋白(nestin)及BrdU表达阳性细胞的数量。结果 rTMS组脑梗死后7、14、21 d mNSS评分明显低于假刺激组及模型组同时间点大鼠(P<0.05),假刺激组及模型组大鼠脑梗死后不同时间点mNSS评分差异不明显(P>0.05)。脑梗死后1d模型组、假刺激组和rTMS组梗死灶周围皮质均可见nestin及BrdU阳性细胞,7 d达高峰。和假刺激组及模型组同时间点相比,rTMS组7、14、21 d nestin及BrdU阳性细胞数量明显增多,两者比较差异明显(P<0.05)。结论 rTMS能促进脑梗死大鼠神经功能恢复,机制可能与rTMS治疗能促进脑梗死周围内源性神经干细胞的激活及增殖有关。     

Astrocytic changes in the hippocampus and functional recovery after cerebral ischemia are facilitated by rehabilitation training

In this study we examined whether astrocytic and basic fibroblast growth factor changes after cerebral ischemia can be influenced by rehabilitation training and if these changes are associated with functional improvement. After receiving either ischemia or sham surgery, male adult Wistar rats were assigned to one of two rehabilitation training group: complex environment housing (EC) or paired housing as controls (CON). Rats were tested in the water maze after 14 days of rehabilitation training. Results showed increased expression of reactive astrocytes (GFAP) in all ischemic animals and in the sham EC rats with a significant overall increased seen in the ischemia EC housed animals. The pattern of basic fibroblast growth factor (FGF-2) expression seen was somewhat similar to that of GFAP. Behavioral data showed that even though all animals learned to perform the water maze task over time, the ischemia CON rats took longer to learn the task while all the ischemia EC animals performed as well as the sham groups. Regression analysis showed that increased GFAP was able to explain some of the variances in the behavioral parameters in the water maze of the ischemia EC rats suggesting that the activation of astrocytes in this group probably mediated enhanced functional recovery. Lastly, it is possible that the favorable effect of astrocyte activation after cerebral ischemia was mediated by FGF-2.     

Impairment and restoration of the endothelial blood-brain barrier in the rat cerebral infarction model assessed by expression of endothelial barrier antigen immunoreactivity

Endothelial barrier antigen (EBA) can be used to detect the blood-brain barrier in the central nervous system of rats. This study investigated the temporal profile of antigen expression in cerebral vessels after infarction and assessed the relationship between re-establishment of this antigen in newly formed vessels and astrocytes around these vessels. Rats were subjected to cerebral ischemia for 2 h by the intraluminal thread method, then killed after 1, 3, 7, 14 and 28 days. Perfusion-fixed paraffin-embedded brains were immunostained for detection of EBA and glial fibrillary acidic protein (GFAP) by the streptavidin-biotin-peroxidase complex method. EBA immunostaining in vessels in the infarcted lesion was reduced at day 1 and had almost disappeared by day 3. Newly formed vessels were found from day 3, but were not stained at day 7. However, these new vessels were weakly stained at day 14 and definitely stained at day 28. GFAP immunostaining was completely negative around these proliferating vessels. The temporal profile of disappearance and re-expression of EBA in cerebral infarcted lesion may be associated with aggravation and improvement of brain edema, although barrier permeability was not explored in this study. The expression of this antigen has no relationship to the formation of astrocyte/endothelial contacts. Received: 4 March 1999 / Revised, accepted: 28 June 1999     

行为训练对双侧海马梗死大鼠学习记忆与NCAM的影响

目的探讨行为训练对双侧海马梗死大鼠空间学习记忆功能恢复及海马神经细胞粘附因子(NCAM)的影响及其作用机制。方法30只SD大鼠采用光化学诱导法制作双侧海马CA1区梗死模型,于24h后随机分为行为训练组和制动组,于造模3d后分别给予行为训练或制动,在大鼠造模后3d、行为训练后7d、14d和21d时进行学习记忆能力测试。并于不同时间取脑进行免疫组织化学染色,观察其梗死灶海马周围NCAM含量的变化。结果行为训练组学习记忆能力评估均优于制动组(P<0.05),海马NCAM含量均较制动组增多。结论行为训练可促进大鼠空间学习记忆能力的恢复,其作用机制可能与海马NCAM的增多有关。     

电针对局灶性脑缺血大鼠缺血灶周围区星形胶质细胞的影响

BACKGROUND： Astrocytes react sensitively to cerebral ischemia, causing reactive proliferation and activation, which may contribute to their effect in protecting or injuring neuronal regeneration. Whether acupuncture, as a treatment for cerebral ischemia, regulates the activated state of astrocytes has become a focus of recent investigations. OBJECTIVE： To observe the effects of electroacupuncture （EA） on ultrastructure changes and reactive proliferation of astrocytes in the marginal zone of focal cerebral ischemia in rats. DESIGN, TIME AND SETTING： Randomized, controlled animal study. This study was performed at the Experimental Animal Center of Guangzhou University of Traditional Chinese Medicine between December 2007 and July 2008. MATERIALS： A total of 90 male Wistar rats were randomly divided into sham operated, model and EA groups. Each group was subdivided into 1 hour, 1, 3, 7, and 21 days post-cerebral ischemia groups, with six animals for each time point. Rabbit anti-rat glial fibrillary acidic protein （GFAP） and goat anti-rabbit IgG/tetramethylrhodamine isothiocyanate were provided by Beijing Biosynthesis Biotechnology. The G-6805 electric acupuncture apparatus was provided by Shanghai Huayi. METHODS： Heat-coagulation-induced occlusion of the middle cerebral artery was performed to establish a model of focal cerebral ischemia, in the model and EA groups. Middle cerebral arteries were exposed without occlusion in sham operated group. EA was applied immediately after surgery in the EA group, 4/20 Hz, 2.0-3.0 V, 1-3 mA, to Baihui（GV 20） and Dazhui（GV 14）, for 30 minutes. The treatment was performed once a day. The sham operated and model groups did not receive acupuncture. MAIN OUTCOME MEASURES： In the marginal zone of focal cerebral ischemia in rats at different time points after intervention, the ultrastructure changes of astrocytes were observed by using transmission electronic microscopy. GFAP expression in astrocytes was also measured by laser confocal scanning microscopy. RESULTS： Cell swelling and rapid proliferation of astrocytes were observed following cerebral ischemia. In comparison to the model group, the degree of swelling of astrocytes was significantly decreased in the EA group. Compared with the sham operated group at hour 1 post-surgery, there was no significant difference in the expression of average fluorescence intensity of GFAP between the EA and model groups （P 〉 0.05）, while the expression of GFAP in both the EA and model groups increased significantly at days 1, 3, 7 and 21 post-surgery （P 〈 0.01）. The expression of GFAP in EA group was also significantly lower than in the model group （P 〈 0.01, P 〈 0.05）. CONCLUSION： Ultrastructural changes and reactive proliferation of astrocytes appear in the marginal zone of focal cerebral ischemia in rats. EA can relieve the degree of swelling of astrocytes and inhibit GFAP overexpression by activated astrocytes. These effects may be related to its ability to regulate the activated state of astrocytes.     

运动训练后大鼠脑梗死灶周围HMGCoAr水平的变化

目的 探讨运动训练后大鼠脑梗死灶周围3-羟-3-甲戊二酰辅酶A还原酶(HMGCoAr)的表达水平变化和大鼠运动功能恢复的关系。方法 将大脑中动脉闭塞致脑梗死的90只大鼠模型用随机数字表法分为训练组、他汀组和对照组,每组各30只,对训练组和他汀组进行运动训练; 在制模后的3、7、14 d用横木行走试验评定大鼠运动功能; 分别用半定量逆转录-多聚酶链反应和免疫组织化学法测定每组大鼠脑梗死灶周围组织的HMGCoAr-mRNA及其蛋白表达水平。结果 运动训练后训练组和对照组大鼠运动功能评分均增高,3、7和14 d 3次评分均有明显差异(P<0.05); 在制模后7、14 d,训练组的运动功能评分值分别为(5.7±0.2)和(6.8±0.4)分,均高于对照组的(3.6±0.2)和(5.1±0.3)分(P<0.05); 他汀组运动功能评分在以上3个时间点间比较均无明显差异(P>0.05),并在7、14 d均低于训练组和对照组的评分(P<0.05); 3组脑梗死大鼠病灶周围HMGCoAr-mRNA(吸光度)和蛋白[阳性信号密度值(%)]水平均为14 d >7 d,7 d>3 d(P<0.05); 其中他汀组指标(HMGCoAr-mRNA:0.591±0.024,0.764±0.017,0.894±0.012; 蛋白:0.423±0.016,0.519±0.008,0.687±0.001)均>训练组(HMGCoAr-mRNA:0.416±0.043,0.654±0.042,0.765±0.036,蛋白:0.301±0.022、0.425±0.014、0.592±0.003),而后者的相关指标水平也均>对照组(P<0.05)。结论 运动训练可使大鼠脑梗死灶周围HMGCoAr-mRNA及其蛋白表达水平增高,并有利于恢复运动功能。     

Relationship between activated astrocytes and hypoxic cerebral tissue in a rat model of cerebral ischemia/reperfusion

Following cerebral infarction, hypoxic tissues remains in the ischemic cortex for long periods of time. Glial fibrillary acidic protein (GFAP) is a specific marker of astrocytes, which is thought to be essential for neuronal survival. We aimed to clarify the relationship between hypoxic tissue and astrocytes following cerebral infarction. Rats with middle cerebral artery occlusion were randomly divided into a 1.5-hour ischemia-reperfusion(1.5-hour IR) group and a permanent ischemia (PI) group. Hypoxic tissue and GFAP fluorescence intensity in the ischemic cortex were observed postoperatively on days 1, 3, 7, and 14. Results showed that hypoxic tissue was present from day 1 to 14 in the 1.5-hour IR group and on days 1 and 3 in the PI group. The GFAP fluorescence intensity in the 1.5-hour IR group was stronger than that in the PI group at the same time point of observation. Over time, GFAP expression increased and peaked at 7 days in each group, followed by a decrease in signal. In hypoxic tissue, the GFAP fluorescence intensity was stronger than that in the surrounding tissue at all observation time points. These data indicate that astrocytes were strongly activated in hypoxic tissue induced by temporary ischemia followed by reperfusion. The activation of astrocytes may partially contribute to the survival and repair of hypoxic tissue following brain ischemia.     

RNA干扰抑制NgR表达对脑梗死大鼠皮质脊髓束可塑性的影响

目的研究应用RNA干扰技术下调Nogo受体(NgR)基因的表达对脑梗死大鼠神经功能恢复及皮质脊髓束可塑性的影响。方法线栓法制作左侧大脑中动脉闭塞脑梗死大鼠模型,用携带U6启动子和NgR特异短发夹RNA(shRNA)编码序列的质粒pNgR-shRNA1、pNgR-shRNA2行缺血侧侧脑室注射给药,以含非特异性shRNA编码序列的无关质粒pGenesil-Con(pCon)注射组及模型组作为对照,应用改良的神经功能缺损评分(mNSS)进行神经功能评定,Western blot检测梗死灶周围脑组织NgR的表达,免疫组织化学技术检测梗死灶周围脑组织生长相关蛋白43(GAP-43)的表达,生物素化葡聚糖胺(BDA)顺行示踪法观察皮质脊髓束可塑性变化。结果 pNgR-shRNA1组、pNgR-shRNA2组mNSS评分明显低于pCon组及模型组(P<0.05),pCon组及模型组mNSS评分差异不明显(P>0.05)。与pCon组及模型组相比,pNgR-shRNA1组、pNgR-shRNA2组梗死灶周围脑组织NgR的表达显著降低(P<0.05),GAP-43的表达明显增强(P<0.05),BDA顺行示踪见病变侧大脑脚水平及病变对侧C1-3脊髓水平BDA阳性纤维数量明显增多(P<0.05)。结论 RNA干扰抑制NgR表达能促进脑梗死大鼠皮质脊髓束可塑性改变及神经功能恢复。     

不同电刺激对卒中后大鼠神经前体细胞增殖的影响

目的 探讨不同部位电刺激治疗对脑卒中后大鼠神经前体细胞增殖的作用.方法 选择2～3月龄,体质量80～120 g雄性SD大鼠95只,随机分为梗死灶周围电刺激组(A组)、肢体电刺激组(B组)、对照组(C组)和假手术组(D组).建立大脑中动脉闭塞模型,在术后24 h开始对两电刺激组大鼠头皮和肢体电刺激治疗.在梗死后7d、14d、21 d、28 d以横木行走试验(BWT)进行神经功能评分,同时进行室管膜和室管膜下5-溴脱氧尿嘧啶核苷(Brdu)的免疫组织化学检测.结果 A组及B组缺血后室管膜Brdu的表达与C组比较在7、14d差异均有统计学意义(P＜0.05),MCAO后7d二者相比Brdu 在室管膜和室管膜下区的表达差异有统计学意义(P＜0.05);MCAO后21dA组Brdu的表达和C组差异有统计学意义(P＜0.05),但此时B组和C组差异无统计学意义(P＞0.05);在MCAO后第1天及第28天三者之间的Brdu均有表达但差异无统计学意义(P＞0.05).结论 电刺激促进MCAO后神经干细胞的增殖,但梗死灶周围头皮电刺激治疗较肢体电刺激治疗引起的神经干细胞增殖明显.     

炎症反应在脑动脉微栓子导致的大脑神经元损伤机制中的作用

目的:探讨炎症反应在脑动脉微栓子导致的大脑神经元损伤机制中的作用.方法:48只SD大鼠随机分为微栓子3 d组、微栓子7 d组、假手术3 d组和假手术7 d组 (均n=12).微栓子组将25～50 mm全血凝块微栓子注入SD大鼠左侧颈内动脉,建立脑梗死阈值下微栓子导致的脑损伤模型.损伤后3 d和7 d分批处死大鼠,CD1...