灯盏花素对大鼠颅脑损伤脑组织线粒体ATP酶活性的影响

目的 探讨灯盏花素对创伤性颅脑损伤后脑组织线粒体ATP酶活性水平的影响。方法 建立自由落体脑挫裂伤模型,伤后立即腹腔注射灯盏花素注射液,采用生化检测的方法分别测定伤后4h、24h和48h及各自的对照组大鼠脑组织线粒体ATP酶活性水平。结果 颅脑损伤后大鼠脑组织线粒体Na~ -K~ ATP酶,Ca~(2 )-ATP酶及Mg~(2 )-ATP酶活性均明显下降(P<0.05),灯盏花素治疗后24h和48h脑组织线粒体ATP酶活性均高于各自时间点对照组(P<0.05)。结论 灯盏花素可以通过影响线粒体功能而减轻创伤性颅脑损伤后的继发性脑损害,从而改善预后。     

大鼠脑出血后血肿周围组织线粒体功能变化的研究

目的:研究大鼠脑出血后脑组织线粒体功能的变化。方法:以50 μL鼠尾血注入大鼠尾状核制作大鼠脑出血模型,注血后分别于12 h及1、3、7 d处死大鼠,断头,取血肿周围脑组织,测定不同时相点血肿周围组织线粒体功能(琥珀酸脱氢酶活性、呼吸控制率)。结果:出血后12 h线粒体呼吸控制率及琥珀酸脱氢酶活性无明显变化,1 d后呼吸控制率较对照组下降,3 d时线粒体呼吸控制率及琥珀酸脱氢酶活性均较对照组下降,出血后7 d线粒体琥珀酸脱氢酶活性、呼吸控制率则较对照组明显下降(P<0.01)。结论:脑出血早期(尤其在12 h之内)血肿周围组织线粒体功能无明显下降,晚期则明显受损。     

选择性NO合成酶抑制剂1400W对创伤后脑组织保护作用的研究

一、材料与方法72只雄性ＳＤ大鼠随机分成生理盐水 (ＮＳ)治疗组和 14 0 0Ｗ治疗组。ＮＳ组又分为 6ｈ、 2 4ｈ、 4 8ｈ、 72ｈ、12 0ｈ、16 8ｈ 6个小组 ,14 0 0Ｗ组分为2 4ｈ、 4 8ｈ、 72ｈ 3个小组 ,每组均为 8只。以 10 %水合氯醛腹腔内注射麻醉 ,采用改进的Ｆｅｅｎｅｙ自由落体脑损伤装置 ,造成右顶叶中度脑挫裂伤模型。伤后 18ｈ给予治疗 ,14 0 0Ｗ组以2 0ｍｇ/ｋｇ体重的剂量腹腔内注射 ,每8ｈ一次 ,ＮＳ组同时给予等量的ＮＳ腹腔注射。二、结果1.每组各时间点ＮＯ测定结果 :见表 1。2 .光镜观察 :ＮＳ组 6～ 2 4ｈ见界限明显的挫…     

脑外伤大鼠水肿区脑组织明胶酶B基因的表达

目的:了解大鼠外伤后脑组织明胶酶B基因表达情况,探讨其与脑水肿发生的关系。方法:40只大鼠,于伤后不同时间取水肿脑组织及正常脑组织;提取组织总RNA;用共扩增逆转录定量PCR方法测定MMP-9基因表达水平。结果:脑外伤水肿区脑组织MMP—9基因表达水平明显高于正常脑组织;伤后12小时表达最强,尔后表达逐渐下降,但仍高于正常对照组。结论:明胶酶B在脑外伤脑水肿形成中可能起重要作用。     

尼古丁对帕金森病小鼠脑组织一氧化氮合酶活性的影响

帕金森病 (ＰＤ)的主要病理变化为黑质纹状体多巴胺(ＤＡ)能神经元变性 ,其病因及发病机制尚不明确。有研究发现 ,应用甲基 苯基 四氢吡啶 (ＭＰＴＰ)制作的ＰＤ小鼠脑组织神经元型一氧化氮合酶 (ｎＮＯＳ)活性增高 ,认为一氧化氮(ＮＯ)参与了ＭＰＴＰ的神经毒作用。某些流行病学及生物学资料表明 ,吸烟对ＰＤ的发病具有保护作用 ,但其作用机制尚不清楚。本实验采用雄性Ｃ5 7ＢＬ小鼠腹腔注射ＭＰＴＰ建立小鼠ＰＤ模型 ,观察尼古丁对ＰＤ小鼠脑组织ｎＮＯＳ活性的影响 ,以探讨尼古丁对ＭＰＴＰ神经毒性的可能保护机制。材料和方法 :选用 8周…     

局灶脑缺血后线粒体ATP酶的活性变化

应用兔大脑中动脉阻断（ＭＣＡＯ）模型，超速离心分离出脑细胞线粒体，生化法测其Ｎａ~＋，ｋ~＋－ＡＴＰ酶，Ｃａ~（２＋），Ｍｇ~（２＋）－ＡＴＰ酶活性，戊巴比妥酸荧光法测其丙二醛含量。结果发现脑缺血后线粒体丙二醛含量显著增加，且随缺血时间的延长而递增；线粒体ＡＴＰ酶（Ｎａ~＋，Ｋ~＋－ＡＴＰ酶、Ｃａ~（２＋），Ｍｇ~（２＋）－ＡＴＰ酶）活性则下降，且随缺血时间延长而递降；相关回归发现线粒体丙二醛含量与ＡＴＰ酶活性之间呈显著负相关。该结果提示脑缺血后线粒体ＡＴＰ酶活性变化参与脑缺血脑水肿的发生发展，其活性变化与自由基反应有关。     

Necrostatin-1对小鼠脑外伤脑组织损害及行为学能力的影响

目的 探讨细胞程序性坏死特异性抑制剂Necrostatin-1(Nec-1)对脑外伤导致的组织损伤和行为学能力(运动功能、学习能力)损害的影响。方法 健康成熟雄性昆明小鼠(体重20～25 g),采用改良的自由落体装置制作定量右侧脑外伤(Traumatic Brain Injury,TBI)模型,建模15 min前同侧脑室分别注射溶剂二甲基亚砜(DMSO)和DMSO配制的Nec-1溶液分别建立脑外伤DMSO组和脑外伤Nec-1组,同时设立假手术组(Sham组),利用行为学试验(Motor Test和Morris水迷宫试验)评估TBI 2周内各组小鼠的运动功能和学习能力损害,利用脑组织缺损体积(Lesion Volume,LV)评价TBI 3周后脑皮质损伤程度。结果(1)脑外伤后1周内能观察到小鼠运动能力评分降低明显(P<0.01),伤后2～7 d各组运动评分均逐渐恢复。与DMSO组比较,Nec-1预给药能明显加快运动功能的恢复过程(P<0.05);(2)所有TBI小鼠与Sham组比较,在水迷宫定位航行试验中搜找平台时需要更长的潜伏期(P<0.05); Nec-1组在伤后第9～12 d表现较短的潜伏期(P<0.05);(3)脑外伤导致各组小鼠脑组织的缺失(P<0.01),与DMSO组比较,Nec-1预处理明显减少了脑外伤后的脑组织损伤体积(P<0.05)。结论 侧脑室预注射Nec-1抑制程序性坏死可减少小鼠脑外伤后脑组织缺损,促进活动功能、学习能力的恢复。     

大鼠脑缺血后脑组织中一氧化氮的变化

本文采用荧光法测定了完全性脑缺血大鼠部分脑区一氧化氮（ＮＯ）代谢产物亚硝酸盐的变化。结果发现，脑缺血后，在大脑皮层、海马及纹状体，均有亚硝酸盐含量的明显升高，以缺血后１０分钟最高，３０分钟时已开始下降，６０分钟时降至正常水平；进一步证实在脑缺血早期具有ＮＯ的急剧升高，其病理生理意义值得进一步研究。     

黄芪注射液对脑出血大鼠细胞凋亡影响的研究

目的 研究脑出血大鼠细胞凋亡的规律及黄芪注射液对出血后脑组织含水量和血肿周围区细胞凋亡的影响.方法 采用肝素化Ⅶ型胶原酶脑内注入法制作大鼠(160只)脑出血模型.制模后根据药物干预的时间随机分成4个治疗组(手术同时组,术后6 h组、12 h组、24 h组,每组32只)和出血对照组(共32只).各治疗组每日经腹腔给予黄芪注射液1次,各组分别于第4 d及第7 d处死.再从上述5组中各选取12只大鼠用于脑组织含水量测定(干湿法),观察不同时间开始治疗对大鼠脑组织含水量、血肿周围区细胞凋亡(脑组织切片TUNEL荧光染色)的影响.结果 治疗组[出血同时组(第4 d)、6 h组(第4 d、7 d)、12 h组(第4 d)]脑组织含水量较出血对照组明显减少(均P<0.01);脑出血后6 h血肿周围凋亡细胞开始出现,3 d达高峰,7 d后明显减少;各治疗组血肿周围细胞凋亡均明显降低,出血同时治疗组和6 h治疗组比24 h治疗组细胞凋亡率明显降低(均P<0.01);脑出血后存在血管内皮细胞凋亡.结论 脑出血后血肿周围神经细胞凋亡是脑出血后继发性神经损伤机制之一;黄芪注射液治疗脑出血,具有减轻脑水肿和神经细胞凋亡作用,以早期用药疗效更好.     

影响脑外伤后生活质量的相关因素研究

目的探讨影响脑外伤（TBI）后生活质量的相关因素。方法选择52例成年TBI患者,进行生活质量评定与分析。结果TBI患者总体生活质量较一般人群差,独立性、心理健康和躯体健康对生活质量的影响最大。在单因子中,以疼痛不适、消极感受、工作能力等方面尤为突出。受伤原因、受伤后病程、GCS评分、消极应对、积极情感等因子与生活质量有关。结论TBI患者生活质量在生理维度、心理和社会功能的各个方面都显著低于一般人群。成熟的应对方式、积极情感有利于提高生存质量。     

Protective effects and time course of Huangqi on early-stage free radical injury following brain trauma in rats★

BACKGROUND： Huangqi （Astragalus mongholicus）, a Chinese herb, has already been included in the ＂Chinese Pharmacopoeia＂ for the treatment of ischemic cerebrovascular disease. Secondary injury following brain injury is associated with free radical production, and Huangqi possesses the ability to ameliorate free radical-mediated injury. OBJECTIVE： This study was designed to observe the correlation between anti-free-radical properties of Huangqi and early histological changes of brain tissues following traumatic brain injury. DESIGN, TIME AND SETTING： This study, a randomized, controlled, animal experiment, was performed from May 2006 to June 2007 at the Experimental Center of Science and Technology, School of Basic Science, Liaoning Medical University, Jinzhou City, Liaoning Province, China. MATERIALS： Healthy, adult, Sprague Dawley rats of either gender were included. Huangqi injection was purchased from Heilongjiang Provincial Zhenbaodao Pharmaceutical Co., Ltd., China （National License Medical Number： Z23020781）. Na^＋-K^＋-adenosine triphosphatase （ATPase）, Ca^2＋-ATPase, and Mg^2＋-ATPase, as well as kits to measure superoxide dismutase （SOD） activity and malondialdehyde （MDA） content, were purchased from Nanjing Jiancheng Biological Reagent Company, China. METHODS： Seventy-two rats were randomly divided into three groups, with 24 rats in each group： （1） sham-operated group： rats were only exposed, but not injured; （2） model group： brain focal laceration rat models were established by free-falling. These groups were intraperitoneally injected with saline, once every 10 hours; （3） Huangqi group： rats were intraperitoneally injected with 4 mL/kg Huangqi （2 g/mL）, once every 10 hours, following brain focal laceration by free-falling. MAIN OUTCOME MEASURES： Ultrastructural changes in brain tissue were observed under an electron microscope 24 hours after injury. The water content of brain tissue was measured using the dry-wet weight method. In additio     

神经节苷脂对脑外伤后脑线粒体呼吸功能和钙泵活性的保护作用

目的研究大鼠脑外伤后脑线粒体功能变化及神经节苷脂ＧＭ１保护作用。方法从牛脑组织中提取ＧＭ１治疗ＳＤ大白鼠自由落体脑外伤，测定脑线粒体呼吸功能变化和线粒体、微粒体质膜钙泵活性变化。结果发现脑外伤后８小时和１６小时脑线粒体Ⅲ态呼吸耗氧速率、呼吸控制率、磷氧比、氧化磷酸化效率及脑线粒体和微粒体质膜钙泵活性低于正常组，差异有显著性意义（Ｐ＜０．０５或０．０１）；经ＧＭ１治疗后上述指标多数有明显上升，并与正常组相近。结论提示脑外伤后脑线粒体呼吸功能有明显障碍，并与线粒体和内质网钙泵活性下降一致；ＧＭ１能显著改善线粒体呼吸功能和提高钙泵活性。     

一氧化碳对局灶性脑缺血脂质过氧化物及Na+-K+ ATP酶的影响

目的　研究一氧化碳对局灶性脑缺血脑组织脂质过氧化物及Na K ATP酶的影响 ,试图从亚细胞水平阐明CO对脑组织保护作用的机理。方法　将SD大鼠随机分为三组 (n =6 ) ,使用HO诱导剂、HO抑制剂腹腔注射为实验组 ,等量生理盐水作为对照组腹腔注射 ,12h后制成MCAO模型。栓塞后 2 4h检测CO浓度、脂质过氧化及Na K ATP酶活性。结果　与对照组相比 ,HO诱导剂组CO浓度明显升高 ,MDA减少 ,SOD及Na K ATP酶增高 (各为P <0 .0 1、P <0 .0 1、P <0 .0 5、P <0 .0 5 ) ,而HO抑制剂组CO浓度明显降低 ,MDA增加 ,SOD及Na K ATP酶活性降低 (各为P <0 .0 0 1、P <0 .0 5、P <0 .0 5、P <0 .0 5 )。HO诱导剂、HO抑制剂对非栓塞侧脑组织脂质过氧化物及Na K ATP酶的活性没有影响 (P >0 .0 5 )。结论　CO是一种信使分子 ,通过减少自由基、增加SOD及Na K ATP酶活性对局灶性缺血的脑组织起保护作用     

缺血再灌注期间大鼠脑线粒体的变化

目的　观察局部脑缺血再灌注对大鼠脑线粒体呼吸链酶复合物活性、过氧化氢 (H2 O2 )产生量和脂质过氧化水平 (MDA含量 )的影响。方法　酶学方法 ,荧光法和比色法。结果　缺血 2 h后复合物 的活性即有明显下降 ,再灌注 30 m in至 4h均无恢复。酶重复合物 活性缺血时无明显变化 ,再灌注 30 m in开始下降 ,一直持续到再灌注 4h。酶复合物 活性在缺血与再灌注期间均无明显变化。缺血再灌注 1h时脑线粒体过氧化氢产生量明显上升 ,再灌注 2 h后又恢复到正常水平。 MDA含量则是在再灌注 2 h开始明显增高 ,4h时仍维持较高水平。结论　缺血再灌注可造成脑线粒体本身氧化损伤。     

Protective effects and time course of Huangqion early-stage free radical injury following brain trauma in rats

BACKGROUND: Huangqi (Astragalus mongholicus), a Chinese herb, has already been included in the "Chinese Pharmacopoeia" for the treatment of ischemic cerebrovascular disease. Secondary injury following brain injury is associated with free radical production, and Huangqi possesses the ability to ameliorate free radical-mediated injury. OBJECTIVE: This study was designed to observe the correlation between anti-free-radical properties of Huangqi and early histological changes of brain tissues following traumatic brain injury. DESIGN, TIME AND SETTING: This study, a randomized, controlled, animal experiment, was performed from May 2006 to June 2007 at the Experimental Center of Science and Technology, School of Basic Science, Liaoning Medical University, Jinzhou City, Liaoning Province, China. MATERIALS: Healthy, adult, Sprague Dawley rats of either gender were included. Huangqi injection was purchased from Heilongjiang Provincial Zhenbaodao Pharmaceutical Co., Ltd., China (National License Medical Number: Z23020781). Na -K -adenosine triphosphatase (ATPase), Ca2 -ATPase, and Mg2 -ATPase, as well as kits to measure superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, were purchased from Nanjing Jiancheng Biological Reagent Company, China. METHODS: Seventy-two rats were randomly divided into three groups, with 24 rats in each group: (1) sham-operated group: rats were only exposed, but not injured; (2) model group: brain focal laceration rat models were established by free-falling. These groups were intraperitoneally injected with saline, once every 10 hours; (3) Huangqi group: rats were intraperitoneally injected with 4 mL/kg Huangqi (2 g/mL), once every 10 hours, following brain focal laceration by free-falling. MAIN OUTCOME MEASURES: Ultrastructural changes in brain tissue were observed under an electron microscope 24 hours after injury. The water content of brain tissue was measured using the dry-wet weight method. In addition, the activity of ATPase and SOD, as well as MDA content, was analyzed using biochemical indicators at 4, 24, and 48 hours after injury. RESULTS: All 72 rats were included in the fmal analysis. At 4, 24, and 48 hours after injury, ATPase activity was significantly reduced in the model and Huangqi groups than in the sham-operated group (P < 0.05), and this was reduction was time-dependent. At four hours after injury, no significant difference in ATPase activity was detected between the Huangqi group and the model group (P> 0.05). At 24 and 48 hours after injury, ATPase activity in the Huangqi group gradually decreased, but remained significantly greater than that in the model group (P<0.05). At four hours after injury, when compared with the sham-operated group, the MDA content in the model group significantly increased and remained at a high level, while SOD activity significantly decreased (P<0.05). In the Huangqi group, MDA content and SOD activity did not change at four hours after injury. However, MDA content significantly decreased, and SOD activity significantly increased, at 24 and 48 hours after injury, compared with the model group (P<0.05). Moreover, at 24 and 48 hours after injury, the water content of brain tissue was significantly lower in the Huangqi group than in the model group (P<0.05). Ultrastructural examination of cerebral cortical neurons revealed severe damage in the model group, compared to the sham-operated group, while only mild injury was observed in the Huangqi group. CONCLUSION: The protective effects of Huangqi against traumatic brain injury correlates with decreasing MDA content and increasing SOD activity.     

注射用丹参多酚酸对大鼠脑缺血再灌注线粒体ATP酶活性的影响

目的探讨注射用丹参多酚酸对大鼠脑缺血再灌注线粒体ATP酶活性的影响。方法将54只雄性SD大鼠随机分成3组(n=18):假手术组(Sham组)、缺血再灌注组(IR组)、丹参多酚酸组(Salvianolate组)。HE染色法观察大脑神经元的组织病理学变化;TTC染色检测脑梗死体积;分光光度计发法线粒体丙二醛含量和线粒体Na~+/K~+ATP酶、Ca~(2+)ATP酶、Mg~(2+)ATP酶活性。结果假手术组大鼠脑组织红染,未见梗死灶;丹参多酚酸组神经细胞变性坏死程度、脑梗死面积较缺血再灌注组明显减轻;与缺血再灌注组相比,丹参多酚酸组线粒体丙二醛含量下降(P0.05)和线粒体Na~+/K~+ATP酶、Ca~(2+)ATP酶、Mg~(2+)ATP酶活性升高(P0.05)。结论注射用丹参多酚酸对缺血再灌注损伤有保护作用,其机制与提高线粒体ATP酶活性有关。     

尼美舒利对大鼠慢性脑缺血损害的保护作用

目的　探讨诱导型环氧和酶 (COX -2 )抑制剂尼美舒利对慢性脑缺血损害的保护作用。方法　大鼠随机分为对照组、缺血组和治疗组 ,治疗组于术后 2 4h开始以尼美舒利 (6mg/kg)每日灌胃 ,连续 60d ,各组于 60d后做病理染色、GFAP免疫组化染色及脑组织内MDA和SOD含量的测定。结果　与对照组相比 ,缺血组GFAP阳性细胞明显增多 ;脑内的SOD含量下降 ,MDA含量增多。治疗组以上变化明显减轻 ,且有显著性差异。结论　COX -2抑制剂尼美舒利对慢性脑缺血损伤有脑保护作用。     

亚低温对大鼠颅脑外伤后脑组织AQP-4和Caspase-3表达的影响

目的观察亚低温治疗对实验大鼠颅脑外伤后水通道蛋白4(AQP-4)和半胱天冬酶3(caspase-3)的影响,探讨亚低温对颅脑外伤后可能的脑保护分子生物机制。方法健康成年雄性Wistar大鼠45只,采用Feeney法建立脑外伤动物模型,随机分为对照组、创伤组和亚低温组,每组15只,亚低温组在损伤后立即给予亚低温暴露,用干湿重法测定脑组织含水量、免疫组织化学法及图象分析技术检测AQP-4和caspase-3及双重染色免疫组织化学法检测AQP-4和S-100。结果与假手术组比较,大鼠颅脑外伤后脑组织AQP-4和caspase-3的表达及脑组织含水量明显升高(P0.05);亚低温治疗后,大鼠脑组织AQP-4和caspase-3的表达及脑组织含水量较脑创伤组明显降低(P0.05)。结论亚低温对创伤性脑损伤的脑保护机制可能与减轻胶质细胞介导的脑水肿,减少神经细胞凋亡有关。