脑栓通抑制凋亡并减轻脑梗死后丘脑继发性损害的研究

目的 研究脑栓通对脑梗死后同侧丘脑继发性损害的神经保护作用及其可能机制。方法 采用高血压大鼠（RHRSP）建立一侧大脑中动脉皮层支闭塞（MCAO）模型,随机分为：假手术组、溶剂对照组和脑栓通组,每组8只。脑栓通组大鼠MCAO术后24h经灌胃给予2ml/kg（10mg/ml）脑栓通,溶剂对照组给予等剂量溶剂,连续6天。MCAO术后1周感觉功能评估后行尼氏染色评价脑梗死灶体积和丘脑损害,并行免疫组化检测丘脑TUNEL、MAP-2和GFAP表达。结果 脑栓通组大鼠患肢感觉功能较溶剂对照组出现明显改善（P〈0.05）。两组间脑梗死灶体积无显著差异（P〉0.05）。脑栓通治疗后同侧丘脑神经细胞数量、MAP-2表达较溶剂对照组显著增多（P均〈0.05）,但GFAP表达显著下降（P〈0.05）。脑梗死后同侧丘脑TUNEL＋细胞数量明显高于假手组,脑栓通可显著减少同侧丘脑TUNEL＋细胞数量（P均〈0.05）。结论 脑栓通能够改善脑梗死后同侧丘脑继发性神经损害和神经功能,其机制可能与抑制同侧丘脑细胞凋亡有关。     

Mechanisms of secondary damage to the thalamic nucleus and substantia nigra in an adult hypertensive rat model following middle cerebral artery occlusion

BACKGROUND: Following ischemia, apoptosis is observed at the ipsilateral ventroposterior thalamic nucleus and substantia nigra, which are distant from, but connected to, the ischemic cerebral cortex, in animals with normotension. However, secondary brain damage in hypertension has not been clearly investigated. OBJECTIVE: The present study determined whether neuronal apoptosis is associated with neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following cortical ischemia in adult hypertensive rats. Results should provide options for determining a time window for anti-apoptotic therapy. DESIGN, TIME AND SETTING: All experimental procedures in this randomized, controlled trial were conducted at the Neurological Laboratory of the First Affiliated Hospital of Sun Yat-sen University of China between October 2006 and July 2008.MATERIALS: Monoclonal primary antibodies specific to mouse anti-rat microtubule-associated protein 2 and glial fibrillary acidic protein were respectively purchased from Sigma Chemical, USA and BD Pharmingen, USA. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) detection kits were purchased from Roche Applied Science, Switzerland and Upstate, USA, respectively.METHODS: A total of 64 male, Sprague Dawley rats, aged 60-90 days, were equally and randomly divided into middle cerebral artery occlusion and sham surgery groups. Renovascular hypertension was established in both groups by renal artery occlusion. Right distal middle cerebral artery occlusion was performed by electrocoagulation in the middle cerebral artery occlusion group. MAIN OUTCOME MEASURES: Microtubule-associated protein 2 and glial fibrillary acidic protein were detected by immunohistochemistry, and apoptotic cells were observed by TUNEL assay. The stainings were separately detected in the ipsilateral ventroposterior thalamic nucleus and substantia nigra.RESULTS: During the 4 weeks following distal middle cerebral artery occlusion in renovascular hypertensive rats, microtubule-associated protein 2 expression gradually, but significantly, decreased (P < 0.05). Expression of glial fibrillary acidic protein increased significantly in the ipsilateral ventroposterior thalamic nucleus and substantia nigra (P < 0.05) and reached a peak at 4 weeks. In addition, number of apoptotic cells was significantly increased in both areas compared with the sham controls (P < 0.05), with a peak at 2 weeks.CONCLUSION: Results suggested that neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following distal middle cerebral artery occlusion in hypertensive rats could be a secondary event resulting from apoptosis. The temporal apoptosis profile provides options for determining a time window for anti-apoptotic therapy at 2 weeks after stroke.     

大鼠大脑皮层梗死后丘脑继发性轴突变性

目的 探讨高血压大鼠大脑皮层梗死同侧丘脑腹后核（ventroposterior nucleus of the thalamus,VPN）继发性轴突变性的病理过程。方法 采用易卒中型肾血管性高血压大鼠（stroke-prone renovascular hypertensive rats,RHRSP）模型制备右侧大脑中动脉皮层支闭塞（middle cerebral artery occlusion,MCAO）模型,作为MCAO组。RHRSP模型仅暴露而不凝闭右侧大脑中动脉皮层支（middle cerebral artery,MCA）,作为假手术组。健康配对的成年大鼠,作为正常对照组。上述3组动物分别在术后1、2、4周3个时间点,行Bielschowsky氏嗜银染色及免疫组织化学染色检测梗死同侧丘脑腹后核βA4淀粉样前体蛋白（amyloid βA4 precursor protein,APP）、生长相关蛋白43（growth associated protein-43,GAP-43）和微管相关蛋白2（microtubule associated protein-2,MAP-2）的表达水平。结果 与同期假手术组相比,在梗死同侧丘脑腹后核,缺血4周时检测到嗜银染色的纤维束明显减少（P <0.05）;APP蛋白在缺血1周时表达开始增强并逐渐增高（P <0.05）,GAP-43蛋白、MAP-2蛋白的表达水平在缺血1～2周开始下降（P <0.05）并持续降低（P <0.05）。结论 轴突标志性蛋白的免疫组织化学检测方法敏感性高、能早期发现丘脑轴突的病理改变,与传统的嗜银染色方法结合,能较全面地评价VPN轴突变性的病理过程。本实验发现梗死同侧VPN的轴突变性是一个慢性进展性的过程。     

长期大脑中动脉闭塞后远隔部位MAP—2和GFAP变化

目的 :探讨长期MCAO后丘脑、黑质网状部 (SNr)微管相关蛋白 2和胶质纤维酸性蛋白的变化。方法 :3 5只SD大鼠分为 7组 ,每组 5只。Tamura法制作动物模型。脑切片分别用鼠脑MAP 2、GFAP抗体 ,ABC法染色。观察丘脑的面积改变 ,SNr面积和长度的改变 ;SNr神经细胞和胶质细胞数的变化。结果 :丘脑面积逐渐缩小 ;SNr面积长度及神经细胞减少 ,胶质细胞增加。脑缺血后 1个月MAP 2减少 ,GFAP增加 ,6个月GFAP丝极消失。结论 :神经细胞减少和胶质细胞增加可能是长期MCAO后丘脑和SNr萎缩的基础     

胰岛素对局灶脑缺血c-jun基因表达的影响

目的观察不同剂量胰岛素对高血压大鼠局灶缺血脑组织ｃｊｕｎ基因表达的影响。方法以肾血管性高血压大鼠（ＲＨＲ）复制大脑中动脉闭塞（ＭＣＡＯ）模型，采用原位杂交技术检测不同剂量胰岛素组和对照组ＭＣＡＯ后３ｈ脑组织ｃｊｕｎ基因的表达。结果与对照组相比，在缺血侧广泛的大脑皮层，低剂量胰岛素组ｃｊｕｎｍＲＡＮ有统计学意义的增加（Ｐ＜００５），而较高剂量胰岛素组ｃｊｕｎｍＲＮＡ增加更为显著（Ｐ＜００１）。结论胰岛素促进缺血脑组织ｃｊｕｎ基因表达可能是其神经保护作用机制之一，而且这种作用呈剂量依赖性。     

Reduction of β-amyloid deposits by γ-secretase inhibitor is associated with the attenuation of secondary damage in the ipsilateral thalamus and sensory functional improvement after focal cortical infarction in hypertensive rats

Abnormal β-amyloid (Aβ) deposits in the thalamus have been reported after cerebral cortical infarction. In this study, we investigated the association of Aβ deposits, with the secondary thalamic damage after focal cortical infarction in rats. Thirty-six stroke-prone renovascular hypertensive rats were subjected to distal middle cerebral artery occlusion (MCAO) and then randomly divided into MCAO, vehicle, and N-[N-(3,5-difluorophenacetyl)--alanyl]-S-phenylglycine t-butyl ester (DAPT) groups and 12 sham-operated rats as control. The DAPT was administered orally at 72 hours after MCAO. Seven days after MCAO, sensory function, neuron loss, and glial activation and proliferation were evaluated using adhesive removal test, Nissl staining, and immunostaining, respectively. Thalamic Aβ accumulation was evaluated using immunostaining and enzyme-linked immunosorbent assay (ELISA). Compared with vehicle group, the ipsilateral thalamic Aβ, neuronal loss, glial activation and proliferation, and the mean time to remove the stimulus from right forepaw significantly decreased in DAPT group. The mean time to remove the stimulus from the right forepaw and thalamic Aβ burden were both negatively correlated with the number of thalamic neurons. These findings suggest that Aβ deposits are associated with the secondary thalamic damage. Reduction of thalamic Aβ by γ-secretase inhibitor may attenuate the secondary damage and improve sensory function after cerebral cortical infarction.     

银杏叶提取物对大鼠脑缺血再灌注后GFAP和细胞凋亡的影响

目的 研究银杏叶提取物(EGb761)对大鼠局灶性脑缺血再灌注后神经细胞凋亡和星形胶质细胞表达的变化.方法 雄性SD大鼠随机分为假手术组、单纯缺血组、EGb761干预组,线栓法建立大脑中动脉缺血再灌注模型(MCAO),原位末端标记(TUNEL)法观察神经细胞的凋亡情况,免疫组化法观测星形胶质细胞的表达.结果 与单纯缺血...     

激肽释放酶促进实验性大鼠大脑皮质梗死后内源性神经干细胞的增殖、迁移和分化

目的 观察外源性激肽释放酶对大鼠皮质梗死后内源性神经再生的影响.方法 用易卒中型肾血管性高血压大鼠,随机分为局灶性大脑皮质梗死+激肽释放酶治疗组、大脑皮质梗死+溶剂对照组和假手术对照组,所有大鼠均腹腔注射5-溴脱氧尿嘧啶核苷(BrdU)用以标记新增殖细胞.分别在不同时间点行神经功能评分后处死大鼠,测脑梗死灶体积,并观察梗死侧侧脑室下区(SVZ)BrdU+、BrdU+/DCX+表达以及梗死灶周BrdU+、BrdU+/NeuN+表达.结果 与溶剂对照组及假手术对照组相比,激肽释放酶治疗促进了术后不同时间点梗死侧SVZ BrdU+、BrdU+/DCX+和梗死灶周BrdU+、BrdU+/NeuN+表达(术后7 d SVZ BrdU+分别为304.0±73.9、167.0±32.2和56.0±12.2,分别q=7.165、12.916、5.751,均P<0.05;SVZ BrdU+/DCX+分别为225.0±13.6、98.0±9.6和23.0±5.6,分别q=30.731、48.735和18.004,均P<0.01;梗死灶周BrdU+为490.0±82.0、308.0±51.5和49.0±9.5,分别q=7.920、19.184、11.264,均P<0.01;术后14 d梗死灶周BrdU+/NeuN+为21.0±3.4和13.0±2.6,t=4.568,P=0.001),并促进了神经功能恢复.结论 外源性激肽释放酶可促进大鼠皮质梗死后内源性神经干细胞活化,并改善神经功能.     

不同时间窗大鼠脑血栓溶解治疗后梗死体积和脑电图的研究

目的：研究不同时间窗脑血栓溶解治疗后脑电变化与梗死体积的关系。方法：应用肾血管性高血压大鼠,用光化学法制成一侧大脑中动脉闭塞模型,在血栓形成后不同时间应用尿激酶静脉溶栓,观察脑电图变化与梗死体积的大小。结果：缺血２小时之内实行溶栓治疗,可缩小梗死性。ＭＣＡＯ３０分钟后溶栓复流后,ＥＥＧ有改善,一小时后慢波减少,２４小时ＥＥＧ可恢复到基本正常。     

脑梗死大鼠神经前体细胞增殖水平的研究

目的研究脑梗死病灶周围及海马处神经前体细胞增殖水平的动态变化。方法采用易卒中型肾性高血压大鼠(RHRSP)，电凝大脑中动脉(MCA)主干制成脑梗死(MCAO)模型。行大鼠神经功能评定，免疫组化观察并计数梗死灶边缘、对侧镜区及双侧海马5-溴脱氧尿核苷(Bromodeoxyuridine，BrdU)标记的细胞。结果MCAO后大鼠神经功能评分减低，5d时恢复正常。MCAO后梗死灶边缘、对侧镜区及双侧海马均有BrdU阳性细胞分布，且病灶侧多于病灶对侧，集中分布于病灶周围。结论脑缺血可诱导神经前体细胞增殖并移向病灶，可能成为脑梗死恢复的重要物质基础。     

Endogenous neurogenesis and neovascularization in the neocortex of the rat after focal cerebral ischemia

The present study was designed to examine whether endogenous neurogenesis and neovascularization occur in the neocortex of the ischemic rat brain after unilateral middle cerebral artery occlusion (MCAO). Sprague-Dawley rats were divided into six groups (n = 29): one control group (n = 4) and five groups composed of animals sacrificed at increasing times post-MCAO (2 days and 1, 2, 4, and 8 weeks; n = 5 per group). To determine the presence of neurogenesis and neovascularization in the ischemic brain, nestin, Tuj1, NeuN, GFAP, Tie2, RECA, and 5-bromo-2'-deoxyuridine (BrdU) were analyzed immunohistochemically. In addition, nestin, GFAP, and Tie2 expression was determined by Western blotting. Triple-labeling of nestin, BrdU, and laminin was performed to visualize the interaction between endogenous neurogenesis and neovascularization. The number of BrdU- and nestin-colabeled cells increased markedly in the neocortex and border zone of the ischemic area up to 1 week after MCAO and decreased thereafter. Western blot analysis revealed that the expression of nestin, Tie-2, and GFAP was amplified in the ipsilateral hemisphere 2 days after MCAO and peaked 1 week after MCAO, compared with that in the normal brain. After ischemic injury, nestin- and BrdU-colabeled cells were observed in the vicinity of the endothelial cells lining cerebral vessels in the ipsilateral neocortex of the ischemic brain. Endogenous neurogenesis and neovascularization were substantially activated and occurred in close proximity to one other in the ipsilateral neocortex of the ischemic rat brain.     

粒细胞集落刺激因子对脑卒中的神经保护作用研究

目的:研究在脑梗塞后不同时间窗内应用粒细胞集落刺激因子(G-CSF)的神经保护作用。方法:中风模型采用线栓MCA法,栓塞后90min后再灌注;动物采用雄性Wistar大鼠(n=45,体重280～320g)。实验组大鼠分别在中风后30min(n=11)、24h(n=12)、48h(n=10)开始皮下注射G-CSF(60ug/kg．day),至第7日结束;对照组大鼠(n=12)应用生理盐水0．3ml/日。每日检测大鼠体重变化。中风后7天,取脑进行形态学研究,分别进行anti-MPA2和TUNEL染色,计算脑梗塞体积和梗塞灶周围神经细胞凋亡情况。结果:对照组脑梗塞体积(163±25mm~3)明显大于30min(81±19mm~3)、24h(98±27mm~3)[P＜0．001]及48h(114±23mm~3)[P＜0．01]等各治疗组。对照组TUNEL阳性细胞数(187±21)明显高于MCAO后30min及24h开始应用G-CSF的治疗组(P＜0．01)。结论:G-CSF有明显的脑保护作用,即使在脑梗塞发生候后48小时才开始应用,效果仍然明显。     

bcl-xl over-expression in transgenic mice reduces cerebral ischemia/reperfusion injury*☆

BACKGROUND： Basal cell lymphoma-extra large （bcl-xl） can inhibit neuronal apoptosis by stabilizing the mitochondrial membrane and suppressing cytochrome C release into the cytoplasm. OBJECTIVE： This study aimed to further investigate the cascade reaction pathway of cellular apoptosis. We established an ischemia/repcrfusion model by middle cerebral artery occlusion （MCAO） in transgenic and wild-type mice, and observed changes in the number and distribution of apoptotic neural cells, differences in cerebral infarct volume, in neurological function score, and in cytochrome C expression in the ischemic cerebral cortex, at different time points, DESIGN AND SETTING： The present gene engineering and cell biology experiment was performed at the Laboratory of Biology, Hubei Academy of Agricultural Sciences and at the Laboratory of Immunology, Tongji Medical College, Huazhong University of Science and Technology. MATERIALS： Male bcl-xl over-expression Kunming mice aged 8 weeks and age-matched male wild-type mice were used for this study. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling （TUNEL） kits were purchased from Boliman, France. Cytochrome C antibody and Bcl-x immunohistochemical kit were purchased from PharMingen, USA and Santa Cruz Biotechnology, USA, respectively. METHODS： Following MCAO and reperfusion, apoptosis in the ischemic cerebral cortex was detected by the TUNEL assay. Prior to MCAO and 3 hours after reperfusion, the Bcl-xl protein level in the ischemic cerebral cortex was measured by immunohistochemistry. At 3, 6, 12 and 24 hours after reperfusion, the level of cytochrome C in the ischemic cerebral cortex was examined by western blot analysis. Subsequent to MCAO, cerebral infarct volume measurement and neurological examination were performed. MAIN OUTCOME MEASURES： Neural cell apoptosis and cytochrome C expression in the ischemic cerebral cortex; cerebral infarct volume and neurological function score. RESULTS： Twenty-four hours after reperfusion, cerebral inf     

大鼠脑梗死后神经前体细胞的增殖及电针作用的实验研究

目的　研究脑梗死病灶周围及海马处神经前体细胞增殖水平的动态变化及电针治疗对其的影响。方法　采用易卒中型肾性高血压大鼠 (RHRSP) ,电凝法凝闭大脑中动脉 (MCAO)。用Garcia等的综合评分法评定大鼠的神经行为学功能 ,免疫组化观察梗死灶边缘、对侧镜区及双侧海马 5 溴脱氧尿核苷 (Bromodeoxyuridine,BrdU)标记细胞的变化。结果　MCAO后大鼠轻偏瘫 ,5天时神经行为学功能恢复正常。MCAO后梗死灶边缘、双侧镜区及双侧海马均有BrdU阳性细胞分布 ,且病灶侧多于病灶对侧 ,病灶周围分布密集。电针治疗促使梗死灶边缘BrdU阳性细胞增多 ,随着治疗时间增加细胞增多更明显。结论　脑梗死可诱导病灶周边及海马神经前体细胞增殖水平上调 ,2周内神经前体细胞随着电针治疗时间的增加而增多。神经前体细胞可能是脑梗死康复的重要物质基础。     

bcl-xl over-expression in transgenic mice reduces cerebral ischemia/reperfusion injury

BACKGROUND:Basal cell lymphoma-extra large (bcl-xl) can inhibit neuronal apoptosis by stabilizing the mitochondrial membrane and suppressing cytochrome C release into the cytoplasm. OBJECTIVE: This study aimed to further investigate the cascade reaction pathway of cellular apoptosis. We established an ischemia/reperfusion model by middle cerebral artery occlusion (MCAO) in transgenic and wild-type mice,and observed changes in the number and distribution of apoptotic neural cells,differences in cerebral infa...     

葡萄糖及胰岛素对高血压大鼠脑梗塞的影响

目的　为研究葡萄糖、胰岛素对高血压大鼠脑梗塞的不同影响。　　方法　采用易卒中型肾血管性高血压大鼠 ,在单侧大脑中动脉闭塞术前半小时分别腹腔注射葡萄糖、胰岛素和生理盐水 ,术后 2 4小时观察动物神经症状并处死动物 ,用光镜进行脑组织病理观察。　　结果　葡萄糖组脑缺血和脑水肿较对照组严重 ,并且伴有皮层下白质出血 ;而胰岛素组脑缺血和脑水肿较对照组轻微 ,未见皮层下白质出血现象。　　结论　葡萄糖可加重脑缺血性损害 ,而胰岛素具有防治脑缺血性损害的作用。     

实验性脑皮层梗死后丘脑netrin-1及其受体的表达

目的观察一侧大脑皮层梗死后远隔丘脑netrin-1及其受体的表达并探讨其可能的作用。方法建立高血压大鼠的右侧大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型,假手术组只暴露而不凝闭MCA,每组24只。MCAO或假手术后第8天和第14天,各组各取12只大鼠处死取脑,分别行梗死侧丘脑免疫荧光和western blot检测netrin-1及其受体DCC、UNC5H2的表达水平和表达部位。结果 MCAO术后第8天netrin-1、DCC和UNC5H2表达开始增加,尤以UNC5H2更为明显,并持续至第14天,双重免疫荧光显示这些蛋白主要在神经细胞上表达。结论Netrin-1及其受体DCC和UNC5H2的表达增高,可能与脑梗死后远隔丘脑的神经可塑性有关。     

降纤酶对大鼠局灶脑缺血／再灌后caspase—3 mRNA表达和细胞凋亡的影响

目的:通过观察降纤酶对大鼠脑缺血损伤后半胱氨酸蛋白酶-3(caspase-3)的表达和细胞凋亡的影响,研究其对脑保护机制。方法:采用大鼠线栓法栓塞一侧大脑中动脉(MCAO)制作局灶脑缺血/再灌注模型,健康雄性Wistar大鼠144只,分为生理盐水组和降纤酶两组,用原位杂交和原位末端标记(TUNEL)方法,观察缺血0、1、3、6和24 h;缺血3 h再灌注3、6和24 h;缺血 6 h再灌注3、6和 24 h的caspase-3 mRNA的表达和 TUNEL染色阳性细胞数。结果:降纤酶保护组caspase-3 mRNA的表达和TUNEL染色阳性细胞数明显少于生理盐水组。结论:降纤酶可抑制大鼠脑缺血/再灌注后caspase-3 mRNA的表达和细胞凋亡。     

Delayed Decompressive Craniectomy Improves the Long-term Outcomes in Hypertensive Rats with Space-occupying Cerebral Infarction

Background and Purpose

No experimental data has been published on the long-term effects of decompressive craniotomy in hypertensive rats with space-occupying cerebral infarction. The aim of the present study was to investigate the efficacy of decompressive craniectomy in a middle cerebral artery occlusion (MCAO) model of hypertensive rats in a prolonged period.

Methods

Totally 92 stroke-prone renovascular hypertensive rats (RHRSP) were subjected to left MCAO by an endovascular occlusion technique. The decompressive craniectomy was performed on 26 RHRSP at 1 and 24 h after MCAO, respectively. Infarct volume, neurological performance, and mortality were evaluated at 1, 2, 4, and 8 weeks after MCAO.

Results

The mortality was reduced from 52.5% in controls to 7.7% and 23.1% in the rats underwent craniectomy at 1 and 24 h after MCAO, respectively (P < 0.05, respectively). All of the treated rats presented smaller infarct volume from 1 week to 8 weeks and better neurological performance at 4–8 weeks after MCAO compared to the controls (P < 0.05, respectively). The craniectomy at early stage was more effective than that at late stage in reducing infarct volume and improving neurological performances at 1 and 2 weeks (P < 0.05, respectively). However, there was no significant difference in infarct volume and neurological scores between the treated groups of rats at 4 and 8 weeks after MCAO (P > 0.05).

Conclusions

Although the early craniectomy is more effective than delayed craniectomy in improving short-term outcome, the latter has the similar beneficial effects as early craniectomy on long-term outcome in hypertensive rats with space-occupying cerebral infarction.     

氟美松对成年大鼠持续性局灶脑缺血后细胞凋亡和Fas基因表达的作用

目的 研究氟美松对成年人局灶性脑缺血后细胞凋亡及相关Ｆａｓ基因表达的作用。方法 健康雄性ＳＤ大鼠随机分成１４组（每组５只）。１～７组为对照组，８～１４组为实验组。用右侧近端大脑中动脉电凝术建立大鼠持续性局灶性脑缺血模型。缺血后１ｈ，实验组动物尾静脉射氟美松（５ｍｇ／ｋｇ），对照组注射生理盐水。分别在缺血后３、６、１２、２４、４８、７２和１２０ｈ取材，用原位末端标记（ＴＵＮＥＬ法）、原位ＲＴ－ＰＣＲ法分别检测缺血后细胞凋亡和Ｆａｓ ｍＲＮＡ表达并进行了半定量分析。结果 氟美松可导致缺血后细胞凋亡提前发生，促进大鼠局灶性脑缺血后Ｆａｓ ｍＲＮＡ的表达，使其表达开始时间提前、表达持续时间延长、表达细胞增多及表达信号增强。结论 氟美松可促缺血后细胞凋亡相关基因Ｆａｓ ｍＲＮＡ的表达，可能是其加重成年大鼠缺血性脑损伤尤其