Effects of Echinacoside on Histio-central Levels of Active Mass in Middle Cerebral Artery Occlusion Rats

Objective To investigate the effects of echinacoside on the extracellular striatal levels of norepinephrine（NE）,dopamine（DA）,homovanillic acid（HVA）,3,4-dihydroxyphenylethanoid acid（DOPAC）,5-hydroxyindoleacetic acid（HIAA）,and 5-hydroxytryptamine（5-HT） in middle cerebral artery occlusion（MCAO rats.Methods The middle cerebral artery was occluded in male Sprague-Dawley rats.Three days later microdialysis probes were placed into the right striatum of MCAO rat brains and the brains were perfused with Ringer＇s solution at a rate of 1.5 μL/min.Cerebral microdialysates were collected every 30 minutes from awake and freely moving rats before assaying for NE,DA,HVA,DOPAC,HIAA,and 5-HT levels by reverse phase HPLC with electrochemistry.Results Three days after MCAO,the extracellular striatal levels of NE,DA,DOPAC,HIAA,HVA,and 5-HT of the MCAO rats increased significantly（at least P0.05 vs.control）.However,simultaneous treatment with echinacoside（30.0 or 15.0 mg/kg） attenuated these increases（at least P0.05 vs.non-treated model rats）.Conclusion These results imply that echinacoside may protect striatal dopa minergic neurons from the injury induced by MCAO and may help prevent and treat cerebral ischemic diseases.

Middle cerebral artery occlusion methods in rat versus mouse model of transient focal cerebral ischemic stroke

Experimental stroke research commonly employs focal cerebral ischemic rat models （Bederson et al., 1986a; Longa et al., 1989）. In human patients, ischemic stroke typically results from thrombotic or embolic occlusion of a major cerebral artery, usually the mid- dle cerebral artery （MCA）. Experimental focal cerebral ischemia models have been employed to mimic human stroke （Durukan and Tatlisumak, 2007）. Rodent models of focal cerebral ischemia that do not require craniotomy have been developed using intraluminal suture occlusion of the MCA （MCA occlusion, MCAO） （Rosamond et al., 2008）. Furthermore, mouse MCAO models have been wide- ly used and extended to genetic studies of cell death or recovery mechanisms （Liu and McCullough, 2011）. Genetically engineered mouse stroke models are particularly useful for evaluation of isch- emic pathophysiology and the design of new prophylactic, neuro- protective, and therapeutic agents and interventions （Armstead et al., 2010）. During the past two decades, MCAO surgical techniques have been developed that do not reveal surgical techniques for mouse MCAO model engineering. Therefore, we compared MCAO surgical methods in rats and mice.

铜砭刮痧联合耳穴压豆对MCAO大鼠脑缺血损伤改善效果及炎性因子的影响

目的 探讨铜砭刮痧联合耳穴压豆对大脑中动脉闭塞(MCAO)大鼠脑缺血损伤改善效果及炎症因子的影响。方法 将50只雄性SD大鼠随机分为假手术组、模型组、刮痧组、耳穴组、联合组,每组10只,采用大脑中动脉线栓法建立MCAO模型。与造模d1开始,对大鼠进行刮痧及耳穴等干预,于干预14 d后,采用mNSS评分表评估大鼠神经功能缺损程度,ELISA检测血清中炎性因子TNF-α、IL-1β、IL-6、IL-10的含量,TTC染色法测定脑梗死面积,Western blot法检测脑组织IL-6、IL-10蛋白含量,RT-qPCR检测IL-6、IL-10 m RNA表达水平。结果 刮痧组、耳穴组、联合组在mNSS评分、脑梗死面积方面均优于模型组(P<0.05)。刮痧组、联合组血清TNF-α、IL-1β、IL-6含量低于模型组(P<0.05),IL-10高于模型组(P<0.05),蛋白含量及mRNA表达IL-6低于模型组(P<0.05),IL-10高于模型组(P<0.05)。耳穴组血清TNF-α、IL-1β、IL-6含量低于模型组(P<0.05),但IL-10含量差异无统计学意义(P>0.05);蛋白含量及mRNA表达IL-6低于模型组(P<0.05),但IL-10差异无统计学意义(P>0.05)。结论 铜砭刮痧联合耳穴压豆可改善MCAO大鼠神经功能,及作用可能与免疫调节机制有关。

P38MAPK磷酸化水平增高参与HPC降低MCAO所致小鼠缺血性脑损伤

目的探讨P38丝裂原激活蛋白激酶(P38 MAPK)磷酸化和蛋白表达水平在低氧预适应(HPC)降低脑中动脉阻塞(MCAO)所致缺血性脑损伤中的变化。方法利用已建小鼠HPC-MCAO模型,将健康雄性BALB/c小鼠随机分为常氧假手术(H0 Sham)、HPC假手术(H4 Sham)、常氧缺血(H0)和HPC缺血(H4)4组,应用2,3,5-氯化三苯基四氮唑(TTC)染色、N issl染色等方法观察脑损伤情况,应用W estern b lot并结合Gel Doc凝胶成像系统,定量检测小鼠脑组织内P38 MAPK磷酸化和蛋白表达水平的变化。结果HPC可明显减小MCAO所致的脑梗死体积(P<0.05)。与H0 sham相比,缺血组小鼠皮层缺血核心区和半影区P38 MAPK磷酸化水平显著升高(P<0.05,n=6),HPC可进一步增加缺血半影区和对侧皮层组织中P38 MAPK磷酸化水平(P<0.05,n=6)。各组间P38MAPK蛋白表达量水平无明显变化。结论P38 MAPK可能参与了HPC降低MCAO所致小鼠缺血性脑损伤的作用。

MCAO模型大鼠学习记忆特征

目的观察MCAO模型大鼠的学习记忆行为学特征。方法对ZeaLonga和Nagasawa法加以改进,采用同侧颈总动脉永久结扎大脑中动脉线栓法制备MCAO模型大鼠,造模1个月后利用Morris水迷宫检测模型大鼠空间学习记忆能力。结果Morris水迷宫定位航行试验结果显示,从第5次游泳训练开始,模型组大鼠的逃避潜伏期[(73.9±50.5)s]和游泳路径[(1631.0±1267.1)cm]显著大于假手术组[(31.6±21.4)s/(677.0±400.9)cm]和正常组[(29.0±20.2)s/(602.0±328.3)cm]大鼠的逃避潜伏期和游泳路径。模型组大鼠空间探索试验中平台象限游泳时间和路径(tP/tT值)与总游泳时间和总路径之比(dP/dT值),[tP/tT值(0.261±0.068)和dP/dT值(0.274±0.054)]显著小于正常组[(0.351±0.065)/(0.352±0.057)]和假手术组[(0.350±0.0662)/(0.349±0.058),P<0.05]。结论同侧颈总动脉永久结扎大脑中动脉线栓法VaD模型大鼠空间学习记忆能力明显下降,与脑缺血记忆障碍特征相似,是研究脑缺血后神经损伤理想的动物模型。

地黄饮子加减方对MCAO模型大鼠HPA轴影响的实验研究

目的:通过对MCAO模型大鼠缺血不同时点及地黄饮子灌胃后HPA轴水平的检测,观察其变化特点及地黄饮子的干预效应。方法:采用放射免疫分析法测定MCAO模型大鼠缺血后6h、48h和灌胃地黄饮子7d后的血浆HPA轴水平。结果:①脑缺血6h时模型组HPA轴水平低于正常组,其功能呈抑制状态;②脑缺血48h时,模型组ACTH、COR的含量较正常组明显升高,CRH含量进一步降低;③地黄饮子能够提高MCAO模型大鼠CRH、ACTH的血浆含量并降低COR的含量。结论:地黄饮子加减方能够提高MCAO模型大鼠CRH、ACTH的血浆含量并降低COR的含量,通过改善HPA轴功能的紊乱在脑缺血急性期发挥保护作用。

大鼠MCAO模型中GST、GSH以及超微结构的改变

目的自由基造成的氧化损伤是卒中后脑损伤的重要原因之一。谷胱甘肽（Glutathione,GSH）,是细胞抵抗氧化应激损伤的重要分子。谷胱甘肽S-转移酶（Glutathione Stransferase,GST）是一组与GSH相关的Ⅱ相酶,与GSH的应用密切相关,而线粒体是细胞内氧化还原反应的重要场所,揭示脑缺血早期不同时间点GST、GSH以及脑细胞内超微结构尤其是线粒体的变化,对阐明脑缺血中自由基造成的氧化损伤机制具有重要的意义。方法本研究在制备大鼠大脑中动脉栓塞（MCAO）模型的基础上,对不同时间点GST蛋白表达、GSH水平以及脑细胞内超微结构的变化进行了观测。结果 MCAO6h后GSH水平出现下降趋势,24~48h后GSH水平明显低于假手术组,GST蛋白表达也明显下降,线粒体出现肿胀、嵴断裂,神经纤维髓鞘结构紊乱,甚至发现部分神经元高尔基体、内质网结构破坏,细胞坏死、液化现象。结论 MCAO早期就已经出现抗氧化能力的下降,表现为线粒体破坏,GSH下降,GST蛋白表达降低。所以缺血性卒中早期提高机体的抗氧化能力以对抗氧化应激会发挥保护神经元、减少脑损伤的作用。

活血荣络片对大鼠MCAO模型脑组织MVD表达的影响

目的:观察活血荣络片对大鼠大脑中动脉缺血(middle cerebral artery occlusion,MCAO)模型脑组织MVD表达的影响。方法:采用线栓法制作SD大鼠MCAO模型,随机分为假手术组、模型组、实验组,对照组,分别在缺血后24 h、3 d、5 d、7 d四个时间点经TTC染色测定脑梗死体积,免疫组化法测定MVD表达。结果:TTC染色测定脑梗死体积显示,对照组、实验组与模型组相比在各时间点梗死体积均有所缩小,差异有统计学意义(P<0.05);实验组与对照组相比,3 d时脑梗死体积缩小明显,有显著统计学意义(P<0.01),余时间点稍缩小,有统计学意义(P<0.05)。MVD表达测定,实验组、对照组MVD单位面积内计数在各时间点均较模型组显著升高,差异有统计学意义(P<0.01);与对照组相比,实验组在24 h、3 d时表达增高,有统计学意义(P<0.05);在5 d、7 d时明显升高,差异有显著统计学意义(P<0.01)。结论:活血荣络片可缩小梗死体积,促进脑缺血区MVD增加,其作用机制可能与促脑血管新生有关。

三种线栓制备大鼠MCAO模型的比较

目的:研究三种尼龙线栓对栓塞法制备大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型的影响,并探讨其意义。方法:SD大鼠随机分为自制线栓组,A4级线栓组,A5级线栓组3个组,经颈外动脉插线制备MCAO模型,观察造模手术操作时间、造模成功率、成模大鼠24 h死亡率、脑梗死体积。结果:自制线栓组插栓平均用时(8.23±2.73)min、A4级线栓组(5.40±1.44)min、A5级线栓组(2.70±0.78)min,组间比较差异有统计学意义(P<0.05);自制线栓组、A4级线栓组、A5级线栓组的成模率分别为62.5%、88.9%、97.9%,组间比较差异有统计学意义(P<0.05);自制线栓组、A4级线栓组、A5级线栓组成模大鼠的24 h死亡率分别为6.7%,5.0%,2.2%,组间比较差异无统计学意义(P>0.05);自制线栓组、A4级线栓组、A5级线栓组脑梗死体积百分比分别为(18.82±12.64)%、(20.59±7.35)%、(35.01±8.00)%,组间比较差异有统计学意义(P<0.05),其中A5级线栓组高于其他两组(P<0.05),自制线栓组梗死体积的稳定性较差。结论:A5级线栓组插线用时少、成模率高、脑梗死体积大且一致,能明显提高造模的稳定性,将线栓对MCAO模型制备的影响降到更低。

Experimental Study on the Protection of Agrimony Extracts from Different Extracting Methods against Cerebral Ischemia-Reperfusion Injury

Objective To study the protective effect of agrimony extracts from different extracting methods on cerebral ischemia-reperfusion injury in rats, in order to optimize the extraction scheme of agrimony.Methods Male rats were randomly assigned into seven groups: 1. Sham-operated group, 2. Untreated MCAO group (MCAO), 3. Petroleum ether extract of Agrimonia pilosa treated MCAO group (PEA), 4. Ethyl acetate extract of Agrimonia pilosa treated MCAO group (EAEA), 5. Ethanol extract of Agrimonia pilosa treated MCAO group (EEA), 6. Water extract of Agrimonia pilosa treated MCAO group (WEA), 7. Nimodipine treated MCAO group (NP). Intragastrical drug administration (i.g) was performed at 0 and 6 hours after MCAO.Neurological function tests were performed after reperfusion for 24 hours, then the brain was removed for the evaluations of the cerebral infarction volume (percentage of total brain volume) by immunohistochemistry,histological changes (hematoxylin-eosin staining), Na+/K+-ATPase, Ca2+-ATPase (modified method of Svoboda and Mosinger), mRNA expression of Tumor suppressor gene (P53) and hot shock protein (HSP70)(quantitative real-time PCR).Results The neurological function of MCAO group had significantly higher scores than the sham group (P<0.01). The WEA group showed a significantly lower neurological score than the MCAO group (P<0.05),indicating the protective effect of WEA on neurological deficits. The mean infarction volumes of WEA (13.5±6.6%, F=4.75, P<0.01), EEA (19.90±6.90%, F=5.23, P<0.01), PEA (20.40±5.30%, F=4.68,P<0.01) and EAEA (22.50±10.50%, F=6.25, P<0.05) group were all significantly smaller than that of MCAO group (29.40±6.50%). HE staining demonstrated that, compared to the treated groups, the infarcted cerebral tissue of MCAO group had more swelling neural cells, lighter stained nucleus, fewer and irregularly distributed neurons. The activity of Na+/K+-ATPase and Ca2+-ATPase reduced in the MCAO group (3.67±0.48 U/mg,1.28±0.26 U/mg, respectively), and were significantly higher in WEA group (7.56±0.85 U/mg, F=12.65,P=0.010; 3.59±0.22 U/mg, F=8.32, P=0.041, respectively). The MCAO group showed significantly elevated P53 and HSP70 mRNA expressions compared to the sham group (P<0.01, P<0.05). P53 mRNA expressions in Agrimony extracts treated groups were significantly lower than that of the MCAO group (all P<0.01), with the WEA group showing the greatest difference from MCAO group. The HSP70 mRNA level of the treated groups were not significantly different from that of the MCAO group.Conclusions Treatment using water extracts of agrimony can promote the best functional and metabolic recovery for rat model of cerebral ischemia-reperfusion injury, which maybe relate with the upregulation of energy metabolism in nerve cells after MCAO.

脉络宁对MCAO大鼠的神经保护作用及其抗氧化机制研究

目的:探讨脉络宁对大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)大鼠的抗氧化作用机制。方法:将18只成年SD大鼠随机分成假手术组(control)、模型组(MCAO)、脉络宁组(mailuoning),每组6只。采用线栓法建立大鼠MCAO模型,缺血2 h再灌注24 h。2%2,3,5-氯化三苯基四氮唑(2,3,5-triphenyltetrazolium chloride,TTC)染液测定大鼠脑梗死体积,荧光法测定活性氧(reactive oxygen species,ROS)的含量,吸光度法测定脑组织中丙二醛(malondialdehyde,MDA)含量以及还原型谷胱甘肽(glutathione,GSH),Western Blot法测定半胱氨酸天冬氨酸蛋白酶-3(cysteinyl aspartate specific proteinase-3,caspase-3)、B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)、Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)表达量。结果:脉络宁能显著降低MCAO大鼠神经功能损伤,减少脑梗死体积;能够抑制脑组织中ROS含量以及MDA的生成,显著提高GSH水平;能够抑制Bax、caspase-3的表达,并增加Bcl-2的表达。结论:脉络宁对MCAO大鼠的保护作用可能与其抑制氧化应激及细胞凋亡有关。

Rb1对MCAO脑组织SOD、NO含量的影响

目的观察Ｒｂ１对局灶性脑缺血区ＳＯＤ、ＮＯ含量的影响。方法ｗｉｓｔａｒ大鼠３０只体重３００－３５０ｇ，雌雄兼用，随机分为３组（ｎ＝１０）：①正常对照组（ＳＯ）；②大脑中动脉梗塞对照组（ＭＣＡＯ）；③药物组：２０μｇ／ｋｇ－１Ｒｂ１连续腹腔注射１０天。①②组生理盐水１０ｍｌ／ｋｇ－１连续腹腔注射１０天。于第１０天灌胃后３０ｍｉｎ①组动物处死取脑制成匀浆，②③组行ＭＣＡＯ后３０ｍｉｎ，处死取脑制成脑匀浆。根据ＮＯ与氧生成硝酸盐、亚硝酸盐，硝酸盐与磺酸及奈乙烯二胺酸盐反应为粉红偶氮化合物及酶联免疫吸附实验原理，采用比色法分别测定脑匀浆ＮＯ、ＳＯＤ含量。结果ＳＯ组脑匀浆ＮＯ含量为７．４１μｍｏｌ·ｍｇ－１（蛋白），ＳＯＤ为００２１μｍｇ·ｍｇ－１（蛋白）；ＭＣＡＯ组脑匀浆ＮＯ含量为１４７３μｍｏｌ·ｍｇ－１（蛋白），ＳＯＤ含量为００１９３ｍｇ·ｍｇ－１（蛋白）；Ｒｂ１组ＮＯ为７３６μｍｏｌ·ｍｇ－１（蛋白），ＳＯＤ含量为００２１９ｍｇ·ｍｇ－１（蛋白），各组间比较有显著差异（Ｐ＜０．０１）。结论①Ｒｂ１能降低ＭＣＡＯ区ＮＯ含量，降低ＮＯ含量的原理可能与ＳＯＤ有关。②Ｒｂ１能增加缺血脑组织ＳＯＤ含量。③脑中?

Hypoxic/ischemic preconditioning attenuate PKCδ-medi-ated injury in patients and mice with cerebral infarction

Objective:cerebral ischemic/hypox-ic preconditioning(I/HPC)is an endogenous strategy in which brief periods of sublethal ischemia/hypoxia render neural tissues resistant to subsequent ischemic/hypoxic damage.This phenomenon has been found in the brain,heart,liver,intestine,muscle,kidneys,and lung.How-ever,whether HPC has a protective effect on secondary cerebral ischemic injury or protein kinase Cδ(PKCδ)within ischemic patients and animal models is still un-clear.Methods:using a hypoxic preconditioned mouse model and a middle cerebral artery occlusion mouse mod-el,combined with 2,3,5-triphenyl tetrazolium chloride(TTC)staining,SDS-polyacrylamide gel electrophoresis(SDS-PAGE),and Western blot,we observed changes in infarction size,density,edema ratio,and changes in PKCδand membrane translocation within the ischemic cortex of the middle cerebral artery occlusion(MCAO)mice.Results:HPC can attenuate neurological deficits and cerebral ischemic injuries of mice following MCAO,including decreases in infarct size,edema ratio,densities of infarct area,and neuron loss.In addition,HPC inhib-its PKCδmembrane translocation in the penumbra of the MCAO-induced ischemic cortex.We found that admin-istration of PKCδ-specific inhibitor dV1-1 mimics the neuroprotective effects of HPC,and nonisoform-specif-ic activation of PKC can partially abolish HPC-induced neuroprotection.Ischemic preconditioning decreased the levels of PKCδin the serum of patients with cerebral in-farction and reduced the cerebral nerve damage caused by ischemia.Conclusion:hypoxic/ischemic precondi-tioning attenuates PKCδ-mediated injury in patients and mice.These findings enrich our understanding of the sig-nal transduction mechanism underlying cerebral HPC and provide clues to developing medicine against ischemia/hypoxia-induced cerebral injuries.

远隔缺血预适应通过上调miR⁃21⁃5p减轻脑缺血模型大鼠细胞凋亡

目的:研究远隔缺血预适应(RIPC)对脑缺血模型大鼠的保护作用及分子机制。方法:18只成年雄性SD大鼠随机分为3组:假手术组(sham)、缺血再灌注组(MCAO/R)组、RIPC+MCAO/R组;术前利用间断夹闭双侧股动脉的方法给予大鼠RIPC处理,利用大脑中动脉栓塞法(MCAO)制备大鼠缺血性脑卒中模型,利用转棒实验检测大鼠运动功能,利用TUNEL染色检测缺血区细胞凋亡,利用real time RT⁃PCR检测大脑缺血区皮质中miR⁃21⁃5p及SPRY1和程序性细胞死亡因子4(PDCD4)mRNA的表达。结果:与MCAO/R组大鼠相比,RIPC处理组大鼠运动功能有所改善,皮质细胞凋亡减少。miR⁃21⁃5p表达增加,而SPRY1和PDCD4 mRNA表达下调(P<0.05)。结论:RIPC处理对减轻缺血性脑卒中大鼠miR⁃21⁃5p表达上调,后者通过抑制靶分子SPRY1和PDCD4的表达抑制细胞凋亡。

远隔缺血预适应通过激活HIF-1α/VEGF通路保护大鼠缺血性脑卒中

目的:研究远隔缺血预适应(RIPC)对大鼠脑缺血模型的保护作用及分子机制。方法:30只成年雄性SD大鼠随机分为4组:假手术组(sham)、RIPC组、缺血再灌注组(MCAO/R)组、RIPC+MCAO/R组;术前通过夹闭双侧股动脉给予相应组RIPC处理,利用大脑中动脉栓塞再灌注法(MCAO/R)制备大鼠缺血性脑卒中模型,神经功能评分检测大鼠的神经功能,用2,3,5-三苯四唑氯(TTC)对脑切片进行染色以评估脑梗死的程度。利用real time RT-PCR检测大脑皮质中低氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF) mRNA的表达。结果:与MCAO/R组大鼠相比,RIPC处理组大鼠神经功能缺损症状较轻(P<0.05),脑梗死体积缩小(P<0.01),皮质中HIF-1α和VEGF mRNA的表达表达明显升高(P<0.05)。结论:RIPC处理对减轻缺血性脑卒中大鼠具有保护作用,其分子机制可能与激活HIF-1α/VEGF通路有关。

银杏内酯A和B混合物对大鼠永久性局灶性脑缺血的保护作用

目的研究银杏内酯A和B混合物(ginkgolide A and ginkgolide B,GKAB)对大鼠永久性局灶性脑缺血的保护作用。方法采用大鼠永久性大脑中动脉阻塞(permanent middle cerebral artery occlusion,pMCAO)模型观察GKAB12.5、25、50mg/kgiv给药对脑梗死体积、脑含水量、行为学症状及组织形态学(光镜)的影响。结果GKAB12.5、25、50mg/kgiv给药呈剂量依赖性减少pMCAO大鼠脑梗死体积、降低脑含水量、改善行为学症状及减轻脑组织形态改变。50、25mg/kg组与模型组相比均有显著性差异(P<0.01、0.05)。结论GKAB对大鼠永久性局灶性脑缺血损伤具有保护作用。

补阳还五汤4类有效部位对局灶性脑缺血大鼠脑梗死体积的影响

目的研究补阳还五汤(BYHWD)中生物碱、多糖、苷、苷元4类有效部位对大脑中动脉闭塞(MCAO)后局灶性脑缺血大鼠脑梗死的作用。方法用颈内动脉线栓法建立大鼠局灶性脑缺血模型,检测脑梗死体积,并比较其神经功能行为评分。结果脑缺血6h,模型组脑梗死体积显著增大(P<0.01),神经功能行为评分显著升高(P<0.01);生物碱、多糖、苷、苷元各组脑梗死体积较模型组缩小(P<0.05、0.01);生物碱、苷、苷元和多糖可使MCAO大鼠神经功能行为评分下降(P<0.05、0.01),其中以生物碱和苷的作用较强。结论MCAO后,大鼠脑组织出现梗死,补阳还五汤4类有效部位生物碱、多糖、苷、苷元能减少脑梗死体积,改善脑缺血后神经行为症状。生物碱和苷的抗脑缺血作用较强,这可能是补阳还五汤抗缺血性脑损伤的部分物质基础。

注射用辛芍对大鼠脑缺血再灌注损伤的保护作用和对脑微循环血流量的影响

目的:观察注射用辛芍对大鼠中动脉阻断(MCAO)局灶性脑缺血再灌注损伤及脑缺血局部微循环血流量的影响。方法:采用栓线法建立局灶性脑缺血再灌注模型,观察注射用辛芍(0.31,0.62,1.25g.kg-1)分别对MCAO再灌注大鼠神经行为学、脑梗死率和脑组织超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)活性,丙二醛(MDA)含量及脑组织病理变化的影响;使用相同动物模型,以激光多普勒血流仪监测各药物干预组对大鼠脑微循环血流的影响。结果:注射用辛芍可明显降低或改善MCAO大鼠行为障碍、脑梗死率及缺血所致组织病理改变,提高SOD活力,降低NOS活性及MDA含量,改善缺血大鼠脑微循环。结论:注射用辛芍对实验性脑缺血具有显著的保护作用,其作用机制可能与增强病灶组织抗氧化和改善局部脑微循环血流有关。

三七皂甙对大脑中动脉栓塞性脑缺血的影响

目的观察三七皂甙 (PNS)及三七皂甙单体 (Rb 1、Rg 1)对大脑中动脉栓塞 (MCAO)后脑血流量(CBF)及脑组织超微结构的影响。方法60只Wistar大鼠随机分7组 :其中第7组为假手术对照组 (SO) ;第1组为MCAO对照组 ;第2 ,3 ,4组MCAO前30min及MCAO后即刻分别静脉给予Rg120μg·kg-1,Rb120μg·kg-1 ,Nim5μg·kg-1 ;第5 ,6组分别于MCAO前灌胃PNS200mg·kg-1 及400mg·kg-1 连续10d。结果与MCAO对照组比较Rb 1,Nim ,PNS400mg·kg-1 组 ,CBF明显增高 (P<0.01) ,Rg1 组CBF无明显增加。PNS能明显提高超氧化物歧化酶 (SOD)活力 ,降低一氧化氮 (NO)含量。超微结构显示 ,Rb1,Rg1,PNS和Nim能明显减轻脑缺血性神经元损伤 ,其中Rb1,Nim ,PNS400mg·kg-1组优于Rg1 和PNS200mg·kg-1组。结论Rb1 ,Nim和PNS400mg·kg-1能明显增加MCAO区CBF ,其机理可能与扩张血管有关 ;Rg1不能增加CBF。Rb 1,Rg 1,PNS有减轻脑缺血坏死作用。其机理可能与提高脑细胞内SOD活力、降低细胞内Ca2 +及NO含量有关。

不同时间窗高压氧对脑缺血-再灌注大鼠模型学习记忆功能的影响

目的观察不同时间窗高压氧治疗(HBOT)对脑缺血-再灌注(I/R)损伤后学习记忆功能的影响,探讨其可能的机制。方法制备大鼠可逆大脑中动脉阻塞脑损伤模型。分别于再灌注后6及24h起始HBOT,观察空间学习记忆功能,计算梗死百分比,免疫组化检测鼠脑iNOS、ChAT,及Bcl-2、Bax表达阳性神经元。结果与缺血对照组比较,早期治疗组大鼠学习记忆功能显著改善;脑梗死比率显著缩小(P<0.01);海马CA1区ChAT阳性神经元增多,iNOS表达减少,且Bcl-2表达增多(均P<0.01),Bax阳性神经元数无明显变化。晚期治疗组显示与早期治疗组改变相似,但iNOS、Bax表达无明显差异。结论早期或延迟HBOT均可改善大鼠脑I/R损伤引起的学习记忆功能不良,显示有神经保护作用。