剥夺异相睡眠后大鼠游泳速度的变化

目的：取消异相睡眠后大鼠游泳速度的变化，为运动训练提供一定的科学方法。方法：2003-04在兰州医学院解剖教研室采用小平台法建立24，48．72h异相睡眠剥夺(paradoxical sleep deprivatlon，PSD)大鼠动物模型。应用Morris水迷宫测试系统自动记录大鼠游泳速度。数据采用SPSS10．0统计软件进行单因素方差分析，两两比较用student-Newman-Keuls(SNK)法。结果：异相睡眠剥夺24，48，72h组大鼠的游泳速度分别为(24．79&;#177;1．50)，(27．73&;#177;489)，(28．21&;#177;2．95)cm／s，比同时段的大平台组[分别为(20．85&;#177;3．491．(21．13&;#177;2．78)，(19．85&;#177;3．64)cm／s]及其正常对照组[分别为(1995&;#177;3．19)．(20．13&;#177;6．13)．(22．94&;#177;3．91)cm／s]快并始终保持在较高水平，其差异有显著性意义(P&;lt;0．05)。而在异相睡眠剥夺24．48，72h组间随着剥夺时间的延长，其游泳速度逐渐增强，但增加幅度逐渐减少。结论：在一定时间段内，剥夺异相睡眠可以提高大鼠游泳速度。     

剥夺异相睡眠后大鼠游泳速度的变化

目的:取消异相睡眠后大鼠游泳速度的变化,为运动训练提供一定的科学方法。方法:2003-04在兰州医学院解剖教研室采用小平台法建立24,48,72h异相睡眠剥夺(paradoxicalsleepdeprivation,PSD)大鼠动物模型。应用Morris水迷宫测试系统自动记录大鼠游泳速度。数据采用SPSS10.0统计软件进行单因素方差分析,两两比较用student-Newman-Keuls(SNK)法。结果:异相睡眠剥夺24,48,72h组大鼠的游泳速度分别为(24.79±1.50),(27.73±4.89),(28.21±2.95)cm/s,比同时段的大平台组犤分别为(20.85±3.49),(21.13±2.78),(19.85±3.64)cm/s犦及其正常对照组犤分别为(19.95±3.19),(20.13±6.13),(22.94±3.91)cm/s犦快并始终保持在一较高水平,其差异有显著性意义(P<0.05)。而在异相睡眠剥夺24,48,72h组间随着剥夺时间的延长,其游泳速度逐渐增强,但增加幅度逐渐减少。结论:在一定时间段内,剥夺异相睡眠可以提高大鼠游泳速度。     

睡眠剥夺对大鼠胃排空及胃肠激素的影响

目的:探讨睡眠剥夺对大鼠胃排空及胃肠激素的影响。方法:接随机数字法将SD大鼠分为:单独笼养组,睡眠剥夺1d组,3d组,5d组,7d组和对照组,各组8只。采用小站台水环境法建立大鼠睡眠剥夺模型。用放射性核素99Tcm灌胃测定大鼠胃液体排空率,用放射免疫法测定胃黏膜中胃泌素、胃动素、生长抑素水平。结果:睡眠剥夺条件下可导致胃排空障碍,大鼠睡眠剥夺3d,5d,7d组胃排空率分别为(72±4)%,(71±5)%,(70±6)%。分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显降低(t=2.763～3.684,P均<0.01)。同时胃肠激素水平发生改变,在睡眠剥夺3d,5d,7d大鼠胃黏膜中胃泌素含量分别为(268±118),(306±151),(405±164)ng/L分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显升高(t=2.104～4.787,P<0.05～0.01)。胃动素含量分别为(51±32),(43±28),(36±20)ng/L,分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显降低(t=2.054～3.062,P<0.05～0.01)。生长抑素水平分别为(219±110),(260±78),(236±88)ng/L,分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显升高(t=2.023～3.120,P<0.05～0.01)。结论:睡眠剥夺可导致胃排空障碍和胃粘膜中胃泌素、胃动素、生长抑素含量发生变化。     

剥夺异相睡眠对大鼠空间参考记忆的影响

目的：探讨异相睡眠与学习记忆的关系。方法：45只雄性Wistar大鼠进行连续4d的Morris水迷宫空间记忆学习任务训练后，立即随机分为：24，48，72h3组，其中所有的剥夺异相睡眠(paradoxical sleep deprivation，PSD)组、正常对照组(CC组)及大平台组(TC组)在第4天最后1次训练结束后立即分别放入睡眠剥夺箱、大平台水箱和普通鼠笼。24，48和72h后，分别将各组大鼠再次任意选取两个入水点，每个点连续两次寻找平台，来衡量空间参考记忆和空间工作记忆的变化。此时平台所处的位置与学习训练时相同。整个行为学研究过程由水迷宫测试系统记录游泳轨迹和相关参数。结果：①随着训练次数的增加，全部大鼠寻找水下平台的能力不断提高。表现为大鼠逐次各点第1次寻找水下平台的游泳探索距离值逐渐减小。②PSD各组大鼠与配对的TC组及CC组相比较，其各点第1次寻找水下平台的游泳探索距离值随剥夺异相睡眠时间延长而延长[72h时为(2368．19&;#177;85．15)，(725．46&;#177;18．46)，(717．83&;#177;17．37)cm]，PSD组游泳距离较CC组和TC组长，其差异有显著性意义(P&;lt;0．001)：TC,CC组大鼠之间其参数统计差异没有显著性意义(P&;gt;0．05)。结论：异相睡眠与学习记忆有关，PSD对大鼠空间参考记忆有损害。     

维生素E干预对静脉补铁慢性肾脏病大鼠氧化应激的影响

目的观察维生素E干预对静脉补铁慢性肾脏病(CKD)大鼠氧化应激的影响,为CKD静脉补铁治疗时进行营养干预,改善机体氧化应激状态提供实验依据。方法采用腺嘌呤灌胃方法建立大鼠CKD模型后,给予一次性尾静脉注射铁剂,同时给予维生素E干预2周,观察血浆GSH、维生素E、NO、MDA含量的变化。结果肾病对照组与正常对照组血浆GSH、维生素E、MDA均有显著性差异(P<0.05);肾病补铁组血浆GSH、维生素E低于正常对照组,血浆MDA高于肾病对照组(P<0.05);肾病补铁维生素E干预组与肾病补铁组血浆GSH、维生素E、NO、MDA均有显著性差异(P<0.05)。结论维生素E干预可提高CKD静脉补铁大鼠抗氧化能力,对缓解其体内氧化应激有重要作用。     

剥夺异相睡眠对大鼠空间参考记忆的影响

目的:探讨异相睡眠与学习记忆的关系。方法:45只雄性Wistar大鼠进行连续4d的Morris水迷宫空间记忆学习任务训练后,立即随机分为:24,48,72h3组,其中所有的剥夺异相睡眠(paradoxicalsleepdeprivation,PSD)组、正常对照组(CC组)及大平台组(TC组)在第4天最后1次训练结束后立即分别放入睡眠剥夺箱、大平台水箱和普通鼠笼。24,48和72h后,分别将各组大鼠再次任意选取两个入水点,每个点连续两次寻找平台,来衡量空间参考记忆和空间工作记忆的变化。此时平台所处的位置与学习训练时相同。整个行为学研究过程由水迷宫测试系统记录游泳轨迹和相关参数。结果:①随着训练次数的增加,全部大鼠寻找水下平台的能力不断提高。表现为大鼠逐次各点第1次寻找水下平台的游泳探索距离值逐渐减小。②PSD各组大鼠与配对的TC组及CC组相比较,其各点第1次寻找水下平台的游泳探索距离值随剥夺异相睡眠时间延长而延长犤72h时为(2368.19±85.15),(725.46±18.46),(717.83±17.37)cm犦,PSD组游泳距离较CC组和TC组长,其差异有显著性意义(P<0.001)。TC,CC组大鼠之间其参数统计差异没有显著性意义(P>0.05)。结论:异相睡眠与学习记忆有关,PSD对大鼠空间参考记忆有损害。     

睡眠剥夺对大鼠胃排空及胃肠激素的影响

目的：探讨睡眠剥夺对大鼠胃排空及胃肠激素的影响。方法：接随机数字法将SD大鼠分为：单独笼养组，睡眠剥夺1d组，3d组，5d组，7d组和对照组，各组8只。采用小站台水环境法建立大鼠睡眠剥夺模型。用放射性核素^99Tc^m灌胃测定大鼠胃液体排空率，用放射免疫法测定胃黏膜中胃泌素、胃动素、生长抑素水平。结果：睡眠剥夺条件下可导致胃排空障碍，大鼠睡眠剥夺3d，5d，7d组胃排空率分别为(72&;#177;4)％，(71&;#177;5)％，(70&;#177;6)％。分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显降低(t=2．763-3．684，P均&;lt;0．01)。同时胃肠激素水平发生改变，在睡眠剥夺3d，5d，7d大鼠胃黏膜中胃泌素含量分别为(268&;#177;118)，(306&;#177;151)，(405&;#177;164)ng／L分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显升高(t=2．104-4．787，P&;lt;0．05-0．01)。胃动素含量分别为(51&;#177;32)，(43&;#177;28)，(36&;#177;20)ng／L，分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显降低(t=2．054-3.062，P&;lt;0．05—0．01)。生长抑素水平分别为(219&;#177;110)，(260&;#177;78)，(236&;#177;88)ng／L，分别与单独笼养组、对照组及睡眠剥夺1d组比较均明显升高(t=2．023-3．120，P&;lt;0．05-0．01)。结论：睡眠剥夺可导致胃排空障碍和胃粘膜中胃泌素、胃动素、生长抑素含量发生变化。     

被动吸烟对急性睡眠剥夺大鼠行为的影响

背景：睡眠剥夺是一种在特殊职业环境中存在的特殊生理心理反应，目前不少人认为香烟烟雾能有效缓解睡眠剥夺后产生的低靡精神状态和异常情绪波动，暂时减轻睡眠剥夺对行为、情绪的不良影响。至今有关香烟烟雾对人体各方面危害的研究已较全面，但有关在急性睡眠剥夺情况下被动吸烟对行为和情绪状态的影响，目前争论颇多。目的：探讨被动吸烟对急性睡眠剥夺大鼠行为、情绪的影响。设计：完全随机分组设计，随机对照实验。单位：解放军第四军医大学基础部教学实验中心及预防医学系放射医学教研室。材料：实验于2004-04／06在第四军医大学基础部教学实验中心完成。选择成年鼠龄3个月、雄性、健康SD大鼠49只，体质量（180&;#177;15）．g，随机分为5组：睡眠剥夺＋被动吸烟24h组（n=8），睡眠剥夺24h组（n=8），睡眠剥夺＋被动吸烟54h组（n=8），睡眠剥夺54h组（n=8），空白对照组（n=17）。方法：①睡眠剥夺＋被动吸烟24h组，睡眠剥夺24h组，睡眠剥夺＋被动吸烟54h组，睡眠剥夺54h组，分别采用小平台水环境法进行24h和54h睡眠剥夺，睡眠剥夺＋被动吸烟24h组和睡眠剥夺＋被动吸烟54h组在睡眠剥夺同时进行被动吸烟，每日12次，120min／次，每次同时点燃3支香烟（有滤嘴香烟），自燃至灰烬。②采用旷场实验测试大鼠的情绪、行为变化：用摄像仪跟踪记录大鼠在旷场中5min内的活动情况，计算并记录大鼠5min内在旷场中距旷场中心的平均距离和运动的总距离，分别考察大鼠的探索性行为及兴奋性状态。距旷场中心的平均距离越近，说明大鼠的探索性行为越多，兴奋性越高；运动总距离越长，也说明大鼠的兴奋性越高。③所有数据以x&;#177;s表示，所用方法为非参数秩和检验，以P〈0．05为有统计学意义。主要观察指标：以各组大鼠旷场实验中距旷场中心的平均距离和运动总距离的比较，观察各组大鼠行为和情绪的变化。结果：纳入大鼠49只，最终进入结果分析49只，无脱失值。①大鼠情绪状态观察结果：实验结束后观察显示，睡眠剥夺＋被动吸烟24h组较睡眠剥夺24h组，睡眠剥夺＋被动吸烟54h组较睡眠剥夺54h组，睡眠剥夺54h组较睡眠剥夺24h组情绪低靡，蜷缩喜静，对外界刺激不敏感，反应冷漠，对其他鼠的攻击行为较少。②旷场实验测试结果：睡眠剥夺24h组距旷场中心的平均距离明显小于空白对照组及睡眠剥夺＋被动吸烟24h组[（53．93&;#177;1．83，58．21&;#177;4．45，58．11&;#177;1．62）cm,（P〈0．01～0．05）]，睡眠剥夺54h组距旷场中心平均距离明显大于睡眠剥夺24h组[（61．53&;#177;3.02，58．11&;#177;1．62）cm，P〈0．01）]，睡眠剥夺24h组的运动总距离明显大于睡眠剥夺＋被动吸烟24h组及空白对照组[（3310．45&;#177;1445．97，1818．20&;#177;733．25，2338．15&;#177;694．70）cm，（P〈0．01-0．05）]，睡眠剥夺54h组运动总距离明显大于睡眠剥夺＋被动吸烟54h组，小于睡眠剥夺24h组[（2410．70&;#177;548．64,1473．5&;#177;945．89，3310．45&;#177;1445．97）cm,（P〈0．05）]。结论：大鼠的行为和情绪反应随睡眠剥夺时间的延长呈现先兴奋后抑制的趋势，而被动吸烟在整个大鼠睡眠剥夺过程中对大鼠的行为和情绪状态起抑制作用。     

睡眠剥夺对大鼠动脉粥样硬化的影响

目的探讨睡眠剥夺（sleep deprivation,SD）对动脉粥样硬化（atherosclerosis,AS）进程的影响及其机制。方法 50只Wistar AS雄性大鼠随机分为5组（每组10只）：AS组、SD1d组、SD3d组、SD5d组、SD7d组。建立AS大鼠SD模型,制备主动脉组织标本,苏木精伊红（hematoxylin and eosin,HE）染色,光镜观察切片。检测主动脉组织还原型谷胱甘肽（glutathione,GSH）及脂质过氧化物丙二醛（malondialdehyde,MDA）含量、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）及超氧化物歧化酶（superoxide dismutase,SOD）活性。检测血清肿瘤坏死因子α（tumor necrosis factor-α,TNF-α）、高敏C反应蛋白（hypersensitivity-C reactive protein,hsCRP）、白细胞介素6（interleukin-6,IL-6）水平。结果随着睡眠剥夺时间的延长,大鼠AS病变进展逐渐加重。主动脉组织GSH含量逐渐降低,MDA含量逐渐增高,GSH-Px及SOD活性逐渐降低。血清中TNF-α、hsCRPI、L-6水平也在逐渐增高。结论睡眠剥夺可通过引起机体的氧化应激反应及加速炎症发展,从而促进AS进程。     

维生素E联合黄芪注射液对维持性血液透析患者氧化应激的干预效果

目的:探讨维生素E联合黄芪注射液对维持性血液透析患者氧化应激状态的干预效果以及使用安全性。方法:将75例维持性血液透析治疗患者分为维生素E治疗组(A组)、维生素E联合黄芪注射液治疗组(B组)和常规血液透析治疗组(C组)各25例,观察各组患者治疗前后过氧化物歧化酶(SOD)、血清丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、循环晚期氧化蛋白产物(AOPP)的变化及白蛋白(Alb)、血红蛋白(Hb)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)的水平。结果:A组与B组治疗后SOD、MDA、GSH-Px、AOPP较治疗前均有显著改善(P0.05);治疗后,A组与B组血清MDA、AOPP水平较C组低(P0.05),A组与B组血清SOD、GSH-Px水平较C组高(P0.05),并且B组各应激指标的改善程度较A组更为显著(P0.05)。在治疗期间,无血栓、出血等并发症的发生。结论:维生素E联合黄芪注射液可以显著改善维持性血液透析患者氧化应激状态,并且短期应用无副作用。     

Protective effect of vitamin E against ethanol-induced small intestine damage in rats

The role of oxidative stress and inflammatory reaction has been reported in various ethanol-induced complications. The purpose of this study was to evaluate the effect of ethanol-induced structural alteration, oxidative stress, and inflammatory reaction on the small intestine of rats, and plausible protective effect of vitamin E to determine whether it inhibits the abnormality induced by ethanol in the small intestine. Twenty-four male wistar rats were divided into three groups, namely: Control^©, ethanol, and vitamin E treated ethanol groups.After six weeks of treatment, the small intestine length, villus height, crypt depth and muscular layer thickness, oxidative stress, and inflammatory parameters showed significant changes in the ethanol treated group compared to the control group. Vitamin E consumption along with ethanol ameliorated structural alteration of the small intestine and reduced the elevated amount of oxidative stress and inflammatory markers such as protein carbonyl, OX-LDL, IL-6, Hcy, and TNF-α. Furthermore, their total antioxidant capacity was increased significantly compared to that of the ethanol group. These findings indicate that ethanol induces the small intestine abnormality by oxidative and inflammatory stress, and that these effects can be alleviated by using vitamin E as an antioxidant and anti-inflammatory molecule.     

Effects of vitamin E on oxidative stress and membrane fluidity in brain of streptozotocin-induced diabetic rats

Background: Diabetics and experimental animal models exhibit high oxidative stress due to persistent and chronic hyperglycemia, thereby deplete the activity of the antioxidative defense system and thereby promote the generation of free radicals. The current study examined the effects of vitamin E on oxidative stress and membrane fluidity in the brain of diabetes-induced rats. Methods: Sprague–Dawley male rats were randomly assigned to normal and streptozotocin (STZ)-induced diabetic groups. The diabetic groups were fed a vitamin E-free diet, 40 mg vitamin E/kg diet, or 400 mg vitamin E/kg diet. Diabetes was induced with STZ after 3 weeks of the experimental diet, then the rats were sacrificed 9 days later to determine the oxidative stress and cell membrane fluidity in the brain. Results: Dietary vitamin E strengthened the antioxidative defense system with an increased activity of the antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and increased vitamin E content, in the brain of the diabetes-induced exeperimental rats. Accordingly, vitamin E was found to reduce the accumulation of reactive oxygen species (ROS), such as superoxide radical decrease the generation of oxidative damage substances, such as the carbonyl value, increase the membrane fluidity lowered by oxidative damage, and significantly improve the lipid composition. Conclusions: Vitamin E was found to be excellent for strengthening the antioxidative defense system, reducing the generation of ROS and damaging oxidative substances, and maintaining membrane fluidity in the brain of diabetes-induced rats.     

辛伐他汀对高脂血症患者早期氧化应激及循环中维生素E的影响——附30例报告

目的：研究辛伐他汀对高脂血症患者早期氧化应激的抑制作用,评估辛伐他汀抑制氧化应激是否独立于降低胆固醇,及氧化应激改变时维生素E的变化。方法：对30例高脂血症患者（高脂血症组）和20名健康受试者（对照组）,进行治疗前分别测量其血清总胆固醇、尿8-异前列腺素F2ａ和血浆维生素E含量并进行比较。干预治疗时,将30例高脂血症患者随机分为随机饮食组（饮食组）或饮食加服辛伐他汀10 mg/d组（治疗组）各15例,分别在基线、第3日、第30日时测量上述指标并进行比较。结果：与对照组相比,高脂血症组的血清总胆固醇、尿8-异前列腺素F2ａ含量较高,维生素E含量较低（P〈0.05～0.01）。与饮食组比较,治疗组治疗第3日尿8-异前列腺素F2ａ开始减少（P〈0.05）,第30日时,尿8-异前列腺素F2ａ明显减少,而维生素E增多,血清总胆固醇降低（均为P〈0.05）。结论：高脂血症患者应用辛伐他汀,在早期即可降低尿8-异前列腺素F2ａ,减轻氧化应激,且这种作用不依赖于血脂的降低,随着应用时间的延长,亦能降低总胆固醇,增加循环中抗氧化维生素E水平。     

维生素E减轻糖尿病大鼠造影剂肾损害氧化应激的实验研究

目的:探讨维生素E对糖尿病大鼠造影剂肾损害的保护作用及其作用机制。方法:将实验动物分为正常组(N),糖尿病组(DM),造影剂组(CM)和治疗组(T)。检测造影后各组血肌酐(Scr),内生肌酐清除率(Ccr),尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG),并检测肾组织超氧化物歧化酶(SOD)活性、过氧化氢酶(CAT)活性、丙二醛(MDA)含量、诱导型一氧化氮合酶(iNOS)活性。同时留取肾脏作PAS染色并作病理形态学分析。结果:与CM组相比,T组Scr下降(P<0.01),Ccr明显上升(P<0.01),尿NAG下降(P<0.01),而肾脏抗氧化酶活性,包括总超氧化物歧化酶(T-SOD)、CAT明显上升(P<0.05),MDA含量下降(P<0.01),iNOS活性明显下降(P<0.01)。病理形态学发现T组肾组织损害特别是肾小管变性坏死较CM组减轻。结论:维生素E能减轻糖尿病造影剂肾损害,其作用与其减轻糖尿病造影剂肾损害中NO参与的氧化应激反应有关。     

The influence of the serum vitamin C levels on oxidative stress biomarkers in elderly women

OBJECTIVES: To verify if there is influence of the vitamin C blood levels on oxidative stress markers in elderly people. In order to verify it, women from a public retirement home were compared to non-institutionalized ones; all of them were in healthy conditions. DESIGN AND METHODS: Vitamin C, albumin, reduced glutathione, malondialdehyde (MDA), protein carbonyls and delta-aminolevulinate dehydratase activity (ALA-D) were analyzed in older women either from a public retirement home (n=45) or non-institutionalized (n=22). RESULTS: The institutionalized ones showed significant decrease for vitamin C levels (p=0.002), ALA-D and MDA (p<0.05). Correlations were found between vitamin C and both albumin and ALA-D, also between ALA-D and both protein carbonyls and age. CONCLUSIONS: The institutionalized women presented decreased vitamin C, albumin, MDA and ALA-D compared to non-institutionalized. Thus, it could be suggested that vitamin C tends to protect blood thiolic proteins. Moreover, its blood delta-aminoevulinate dehydratase activity seemed to be an additional biomarker of oxidation stress in healthy elderly.     

Evidence of oxidative stress in the renal cortex of diabetic rats: favourable effect of vitamin E

The aim of this study was to determine whether there are any disturbances of red/ox balance in the renal cortex of rats during the course of experimental diabetes. In the renal cortex of rats with streptozotocin-induced diabetes, the activity of superoxide dismutase (SOD) isoenzymes, glutathione peroxidase (GSH-Pox), glutathione S-transferase (GST) and glutathione reductase (GSH-RED) was measured in the 5th, 10th and 15th weeks of diabetes. Free radical cell damage was assessed on the basis of malonyldialdehyde (MDA) concentration. The influence of lipophilic antioxidant vitamin E on these analytes was also studied. An increase in MDA concentration in the 10th and 15th weeks of diabetes correlated significantly with plasma glucose concentration (r = 0.47; p < 0.001). Moreover, MDA concentration was influenced by time (+); p < 0.001, diabetes (+); p < 0.001, vitamin E (-) p < 0.001 (ANOVA). Plasma creatinine concentration in rats was elevated by diabetes (p < 0.001), whereas vitamin E decreased the concentration (p < 0.05). Vitamin E lowered the activity of GSHPox (p < 0.001) and GST (p < 0.01) (ANOVA). Our results indicate that during experimental diabetes, disturbances of red/ox balance lead to disturbance in renal function manifested as increased creatinine blood concentration. We suggest that oral supplementation of vitamin E protects the renal cortex of rats during experimental diabetes.     

Effects of hormone replacement therapy with vitamin C and E supplementation on plasma thyroid hormone levels in postmenopausal women with Type 2 diabetes

Recent studies have shown that hormone replacement therapy (HRT) can exert regulatory affects on lipid and glucose homeostasis. It has been demonstrated that hyperglycemia also involving the formation of lipid peroxides, exert several biological effects that may contribute to the onset and progression of thyroid and kidney abnormalities of postmenopausal women Type 2 diabetes. Therefore, the aim of our study was to evaluate the effect of HRT, vitamin C and E (VCE) treatments on some plasma biochemical and hematological parameters and plasma thyroid hormone levels in postmenopausal women with or without diabetes.     

维生素E防治缺血性心脏病心衰氧化应激状态的动物实验研究

目的　探讨维生素E防治缺血性心脏病心衰效果及其抗氧化应激作用。方法　兔 16只随机分为 3组 :空白对照组 (5只 ) ,结扎冠脉组 (5只 ) ,维生素E组 (6只 )。除空白对照组外 ,其他动物行冠脉结扎手术 ,建立心梗心衰动物模型 ,维生素E组给予维生素E干预性治疗 ,6 0～ 70d后 ,测其血流动力学和氧化应激状态指标 :左室舒张末期压力 (LVEDP) ,左室收缩期峰压 (LVPSP) ,血浆中的脂质过氧化物丙二醛 (MDA) ,超氧化物歧化酶 (SOD) ,谷胱甘肽过氧化物酶 (GSH -PX)及心钠素 (ANP)的水平。结果　① 6 0～ 70d后 ,结扎冠脉组与空白对照组和维生素E组相比 ,前者氧自由基代谢明显失衡 ,表现为 :结扎冠脉组血浆中MDA升高 ,而SOD、GSH -PX明显下降 (P <0 0 5 )。②结扎冠脉组与空白对照组和维生素E组相比 ,心功能明显下降 ,表现为 :结扎冠脉组血浆ANP水平明显高于后两组 (P <0 0 5 ) ,LVEDP高于空白对照组 ,LVPSP明显低于空白对照组 (P <0 0 5 ) ,与维生素E组相比也有相应的变化趋势。结论　维生素E具有氧自由基清除活性 ,有助于阻断缺血性心脏病心衰时氧化应激状态下的恶性循环过程 ,达到一定的治疗效果。     

维生素C和维生素E对移植肺再灌注损伤保护作用的实验研究

目的：观察维生素C（Vit）和维生素E（VitE）对大鼠移植肺再灌注损伤的保护作用。方法：采用大鼠自体左肺模拟原位移植模型，治疗组分别于再灌注前10min静脉注入VitC（200mg/kg）和（或）VitE乳剂（100mg/kg）。再灌注4h后观测移植肺气体交换功能，顺应性，血管通透性，脂质过氧化程度，ATP含量以及组织病理学变化。结果：缺血再灌注（I／R）组移植肺气体交换功能，顺应性降低，脂质过氧化程度增加，ATP含量下降，组织病理学改变明显（P＜0．01）；给药组移植肺气体交换功能，顺应性与I／R组相比无明显改善（P＞0．05），其它指标均有不同程度的改善，以VitC和VitE合用时改善最为显著（P＜0．01）。结论：VitC和VitE对移植肺再灌注损伤具有协同保护作用。     

Antioxidant potential of vitamins A, E and C in modulating oxidative stress in rat brain

Background: Stress is known to affect synaptic plasticity, dendritic morphology and induces neurotoxic damage in humans, probably through generation of free radicals. Both ex vivo antioxidant vitamins and in vivo free radical scavenging enzymes exist. In the present study, restraint stress induced pro-oxidant status of rat brain was evaluated in terms of measurement of glutathione (GSH), lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and free radical scavenging enzymes activities. The efficacy of antioxidant vitamins A, E and C alone and in combination was also evaluated in modulating inherent antioxidant system in stressed rats. Methods: Rats were treated with vit A, E and C alone (15 mg/kg of body weight) and in combination vitamins (E and C) prior to and after 6 h of restraint stress exposure. Both nonstressed and stressed rats were handled simultaneously. Pro-oxidant status of brain tissue was evaluated by determining the levels of GSH, TBARS and activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT). Results: Restraint stress induced a decrease in the level of GSH and the activities of SOD, GST and catalase, while the levels of TBARS were found elevated. Both pre-stress and post-stress vitamin treatments (either alone or combined) resulted in alteration of these parameters towards their controls values with a relative dominance by latter. Vitamin E was found most effective in restoring inherent antioxidant system, no additive effect was observed in combined vitamin treatment as expected. Conclusion: Immobilization of rats generated oxidative stress in rat brain, by decreasing the activities of SOD, GST, catalase and glutathione levels, while increasing the lipid peroxidation. Post stress vitamin E treatment was found most effective than vitamins A and C in enhancing the levels of glutathione and activities of SOD, GST and catalase and decreasing lipid peroxidation. Thus vitamin E can be given as a nutritional supplement for scavenging free radical generated in the brain tissues in order to reduce oxidative stress.