金纳多对突发性耳聋病人血液流变学和血清SOD、LPO的影响

目的 观察金纳多对突发性耳聋病人血液流变学和血清ＳＯＤ活性、ＬＰＯ含量的影响。方法 将１５２例突发性耳聋患者随机分为两组，金纳多治疗组８６例，对照组６６例，检测各组治疗前后血液流变学、ＳＯＤ活性和ＬＰＯ含量。结果 突发必 聋病人金纳多治疗组有效率为８９．５３％，对照组为７４．２４％（Ｐ〈０．０１），经金钠多治疗后血液粘度下降，ＳＯＤ活力提高、ＬＰＯ含量下降，均优于对照组（Ｐ〈０．０５，〈０．０１）     

Increase in ferric and ferrous iron in the rat hippocampus with time after kainate-induced excitotoxic injury

The present study aimed to elucidate the distribution of ferric and ferrous iron in the hippocampus after kainate-induced neuronal injury. A modified Perl's or Turnbull's blue histochemical stain was used to demonstrate Fe3+ and Fe2+ respectively. Very light staining for iron was observed in the hippocampus, in normal or saline-injected rats and 1-day post-kainate-injected rats. At 1 week postinjection, a number of Fe3+-positive, but very few Fe2+-positive, cells were present, in the degenerating CA fields. At 1 month postinjection, large numbers of Fe3+-positive glial cells, and some Fe2+-positive blood vessels, were observed. At 2 months postinjection, large numbers of Fe3+- and Fe2+-positive glial cells were present. The labeled cells had light and electron microscopic features of oligodendrocytes, and were double labeled with CNPase, a marker for oligodendrocytes. The observation of an increasing number of Fe3+- and Fe2+-positive cells in the degenerating hippocampus with time is consistent with the results of a nuclear microscopic study, in which an increasing amount of iron was detected in the degenerating hippocampus after kainate injection. In addition, the present study showed a shift in the oxidation state of the accumulated iron, with more cells becoming Fe2+ at a late stage. A possible consequence of the high amounts of Fe2+ in the hippocampus after kainate injection is that it could promote free radical damage in the lesioned areas.     

Nicotinamide attenuates the ischemic brain injury-induced decrease of Akt activation and Bad phosphorylation

Nicotinamide protects cortical neuronal cells against cerebral ischemic injury through activation of various cytoprotective mechanisms. Here, this study confirmed the neuroprotective effects of nicotinamide in focal cerebral ischemic injury and investigated whether nicotinamide modulates a crucial survival pathway, Akt and its downstream targets. Adult male rats were treated with vehicle or nicotinamide (500 mg/kg) 2 h after the onset of middle cerebral artery occlusion (MCAO). Brains were collected 24 h after MCAO and infarct volumes were analyzed. Nicotinamide significantly reduced the infarct volume in the cerebral cortex. Potential activation was measured by phosphorylation of PDK1 at Ser²⁴¹, Akt at Ser⁴⁷³, and Bad at Ser¹³⁶ using Western blot analysis. Nicotinamide prevented the injury-induced decrease of pPDK1, pAkt, and pBad levels. 14-3-3 levels were not different between vehicle- and nicotinamide-treated animals. However, pBad and 14-3-3 interaction levels decreased during MCAO, but were maintained in the presence of nicotinamide, compared to levels in control animals. These findings suggest that nicotinamide attenuates cell death due to focal cerebral ischemic injury and that neuroprotective effects are mediated through the Akt signaling pathway, thus enhancing neuronal survival.     

吸烟对微循环的影响以及脂质过氧化的中介和自由基清除剂的保护作用

吸烟对微循环的影响以及脂质过氧化的中介和自由基清除剂的保护作用阮瑰＊刘飒＊赵汉青＊张月娥＊张叔伦＊吸烟危害人类健康，全世界因为吸烟导致的相关疾病发病率和死亡率不断增加［１～３］。研究认为，吸烟可以损伤血管内皮，导致心血管疾病［４］。近年来，经实验证明...     

氧自由基在高氧所致离体血管内皮细胞损伤中的作用

本实验研究了离体兔主动脉血管内皮细胞在常压高氧(100%O_2)条件下(0～72h)细胞形态、三磷酸腺苷(ATP)、黄嘌呤氧化酶(XO)活性、丙二醛(MDA)含量及谷胱甘肽过氧化物酶(GSH-px)活性的改变。我们的实验发现内皮细胞形态改变(细胞肿胀、畸形、脱落)呈时间依赖性;ATP含量经短暂的升高后(24h)持续降低(48～72h);高氧作用24～48h内皮细胞XO活性、MDA含量持续升高,72h XO活性、MDA含量开始降低,但仍高于对照组;GSH-px活性在48h内无明显改变,72h其活性升高。上述结果表明高氧确能引起内皮细胞损伤,氧自由基在其损伤过程中有重要作用。     

Nicotinamide induces male-specific body weight loss in the postnatal period through molecular regulation of the hypothalamus and liver

Molecular mechanisms of body weight control have been discovered recently and much research focuses on the hypothalamic regulation of food intake and the hepatic regulation of glucose utility. We previously reported that postnatal nicotinamide treatment reduced brain dopamine and body weight. To further investigate the differential effects of nicotinamide-mediated body weight loss, nicotinamide (i.p. 100 mg/kg) was injected into postnatal and adult mice twice a week for 4 weeks. Interestingly, following nicotinamide treatment, male postnatal mice displayed reduced body weight and spontaneous motor activity. No significant changes were observed in adult and postnatal female mice or adult male mice following nicotinamide treatment. In male postnatal mice, hypothalamic agouti-related peptide (AGRP) and proopiomelanocortin (POMC) levels were increased in the arcuate nucleus following nicotinamide treatment. Neuropeptide Y (NPY) levels were unchanged in both male and female mice. Additionally, nicotinamide-injected male postnatal mice had increased glucose 6-phosphatase (G6Pase) and decreased phosphoenolpyruvate carboxykinase (PEPCK) expression in liver. These results indicate that hypothalamic POMC and hepatic PEPCK are important molecules that mediate nicotinamide-induced weight loss in postnatal male mice.     

力竭游泳后大鼠大脑微循环超微结构与自由基代谢动态变化的同步研究

观察力竭游泳后即刻、24h和48h大鼠大脑微循环超微结构的动态变化，并测定大鼠大脑组织MDA含量、SOD和GSH—px的活性。实验结果表明，力竭游泳后即刻大鼠大脑微循环结构发生明显的变化，24h后较力竭游泳后即刻有所好转，48h后大鼠大脑微循环形态结构恢复接近正常。力竭游泳后观察各时段MDA含量无显著性改变，而SOD的活性在力竭游泳后即刻显著升高，24h后显著下降，48h后又显著上升；GSH—px活性动态变化呈下降趋势，且24h下降具统计学意义，特别是在24h与SOD同步明显下降，表明此时SOD和GSH—px消耗量最大，以及时清除自由基，减轻自由基对脑组织造成的损伤，有利于大脑微循环形态结构的修复。     

脉冲磁场对小鼠血液SOD活性及MDA含量的影响

采用脉冲频率２０Ｈｚ,强度分别为０．２５、０．３、０．６４Ｔ三种不同强度的脉冲磁场对小鼠进行４０ｍｉｎ全身辐射,对照组进行４０ｍｉｎ假辐射。磁处理后即刻取血对其血液的自由基指标（ＳＯＤ比活性、ＭＤＡ含量）进行测量。结果表明辐照强度０．２５Ｔ组与对照组小鼠血液的自由基代谢未改变;０．３４Ｔ组小鼠血液的ＳＯＤ活性的ＭＤＡ含量均显著低于其它组。结果表明低频脉冲磁场对小鼠的自由基影响较大并存在一定的窗口效     

夏至草醇提物对急性微循环障碍大鼠自由基损伤的影响

目的观察夏至草醇提物对高分子右旋糖苷(Dextran 500)致急性微循环障碍大鼠器官自由基损伤的影响。方法Wistar雄性大鼠20只,随机分为夏至草组(n=8)、模型组(n=6)和对照组(n=6)。静注10?xtran 500(10 ml/kg.bw)复制急性微循环障碍模型(对照组以等量生理盐水代替)。6 min后,夏至草组自颈静脉缓慢推注夏至草醇提物(5 g/ml,6 g/kg.bw),其它两组以等量生理盐水代替。40 min后,制备肝、肾、心肌、肺组织匀浆,观察组织匀浆自由基指标的变化。结果与对照组相比,模型组肝、肾、心肌、肺组织匀浆MDA含量显著升高,SOD活性降低;夏至草组各器官组织匀浆MDA含量显著低于模型组,SOD活性升高,除心肌组织匀浆SOD活性低于对照组外,其它各指标与对照组均无统计学意义。结论夏至草醇提物能明显减轻Dextran 500致急性微循环障碍大鼠的自由基损伤。     

延迟预适应对缺血再灌注损伤冠状动脉内皮细胞的保护作用

目的:研究延迟缺血预适应(IPC)对缺血再灌注(I/R)冠状动脉内皮细胞的保护作用。方法:所有动物随机分为三组:假手术组(CON组,n=6),缺血再灌注组(I/R组,n=6),预适应组(IPC组,n=6)。I/R组及IPC组分别于不同时间段抽血检测NO、丙二醛(MDA)及超氧化物歧化酶(SOD)的含量。实验结束后,取心脏左前降支(LAD)所支配的心肌组织一小块,行免疫组化染色。结果:IPC组NO缺血前明显高于开胸后,缺血前IPC组高于I/R组;MDA含量缺血前及再灌注后IPC组均低于I/R组;SOD的活性,再灌注后两组差异显著。IPC组内皮型一氧化氮合成酶(eNOS)的表达明显高于I/R组。结论:延迟预适应早期内皮细胞生成NO的量增加,自由基减少,且保护后期的再灌注中NO、自由基的量处于相对稳定,同时使内皮中SOD的活性及eNOS的表达增加。     

黄芪皂甙抗犬心肌自由基损伤作用

在黄嘌呤－黄嘌呤氧化酶制造的自由基损伤模型上，用引导培养心肌细胞动作电位和离体心脏灌流的方法，发现黄嘌呤－黄嘌呤氧化酶使动作电位的各参数减少，使离体心功能显著下降，而黄芪皂甙可使上述改变向正常方向转化，因此，黄芪皂甙具有抗自由基损伤作用。     

有氧及无氧训练对自由基清除能力的影响

目的　探讨中长跑有氧、无氧训练对自由基产生及清除能力的影响 .方法　对田径队中长跑运动员 ,根据个人运动专长 ,安排相应专项训练 ;12名进行有氧训练 ,14名进行无氧训练 ,分别在训练前及运动后即刻抽静脉血 ,检测与自由基产生及清除有关的ROS、SOD、CAT和乳酸等其他生化指标 .结果　①两组训练后LD、Na水平极显著升高 ,Cu水平极显著下降 (均p <0 .0 1) .②有氧组训练后SOD水平极显著下降 (p <0 .0 1) ,Mg水平显著下降 (p <0 .0 5 ) .③无氧组训练后CAT水平显著下降 (p <0 .0 5 ) ;Ca及Fe水平极显著升高 (p <0 .0 1) .④两组比较 ,无氧组LD、SOD、Na、Fe水平高于有氧组 ;K水平低于有氧组 .结论　①有氧训练对血浆自由基的清除能力明显强于无氧训练组 .②运动后血浆铜离子水平的下降影响SOD活性及血浆自由基的清除 .     

光量子血疗法治疗白塞氏综合征的疗效分析

采用光量子疗法（UBI）对22例白塞氏综合征（BS）病人进行治疗，以11例常规药物治疗的BS病人作为药物组对照疗效。同时检测二组病人治疗前后的超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH－Px）、肿瘤坏死因子（TNF）、脂质过氧化物（Lpo）、丙二醛（MDA）、过氧化氢酶（Cat）、免疫球蛋白、白细胞亚微结构等变化。结果表明，BS患者经UBI治疗后血中SOD、GSH－Px、Lpo有不同程度提高，而MDA、TNF有不同程度下降，白细胞微绒毛明显增多变粗。提示UBI对BS治疗效果优于常规药物，因而UBI是治疗BS的一种有效方法。     

丹参对脊髓损伤早期自由基影响的实验研究

目的通过观察大白兔脊髓损伤模型，早期及使用丹参后的变化，探讨丹参在脊髓损伤早期对自由基的作用机制。方法通过改良的Allen‘s法制作脊髓损伤模型。分别在不同时段测定血液标本和脊髓标本的丙二醛(MDA)和超氧化物歧化酶(SOD)。通过应用丹参观察上述指标的变化，并在光镜下观察组织形态的变化。结果损伤组血液标本和脊髓标本中MDA升高、SOD降低，丹参组血液标本和脊髓标本中MDA有所减低，SOD有所升高，丹参组血液标本和脊髓标本所测定的各个指标与损伤组的比较有显著性差别。组织学形态上，丹参组治疗组脊髓损伤程度小，神经元细胞破坏少。结论脊髓损伤后血液和脊髓组织中氧自由基含量升高，丹参能有效清除自由基，从而保护脊髓，在一定程度上阻止继发损伤的进一步发展。     

Iron induces oxidative stress and may alter the rate of aging in the housefly, Musca domestica

Iron is known to play a catalytic role in the generation of oxygen free radicals in vitro. The present study was conducted in order to determine the in vivo effects of iron intake. Administration of 2 mM ferrous chloride to adult male houseflies in their drinking water significantly shortened their life span, increased the concentration of inorganic peroxides and chloroform-soluble fluorescent material, and stimulated the activity of catalase. Levels of superoxide dismutase activity, glutathione and oxygen utilization were unaffected. Overall, these results indicate that iron causes oxidative stress in vivo and may influence the rate of aging.     

在培养的心肌细胞中锌的抗氧自由基损伤作用的观察

本文通过向培养基中加入黄嘌呤和黄(?)呤氧化酶系统成分造成培养的心肌细胞受氧自由基伤害,以电生理的改变和BaCL_2引起心肌细胞停搏的闭浓度为指标,观察了微量元素Zn的抗氧化损伤作用。结果示:XOD组与对照组比较,动作电位APA、OS、MDP、TP、Vmax及APD_(50)各电参数明显减小。BaCl_2引起心肌细胞停搏的阈浓度亦减低。而加Zn组与对照组比较,以上结果除TP值偏低P<0.05外,其它参数则无显著性改变。加Zn组与XOD组相比,动作电位各电参数明显增大,BaCl_2引起心肌细胞停搏的阈浓度亦增高。提示Zn对培养的心肌细胞氧自由基所致的损伤具有保护作用。     

进入高原血粘度增高与红细胞增多及自由基的关系

目的 :探讨进入高原人血粘度增高与红细胞增多及自由基反应之间的关系。方法 :对居平原战士、进入高原 1年和进入高原 1个月的平原籍战士静息时的血液流变学指标和全血SOD 1进行检测。并对进入高原 1个月的平原籍战士运动前、运动后即刻和运动后 1h的血液流变学指标和全血SOD 1进行检测。结果 :进入高原 1个月和 1年战士组血液粘度、红细胞压积逐步升高 ,而全血SOD 1逐步下降 ,进入高原 1年战士组和平原战士组比较相差非常显著 (P <0 .0 1) ;进入高原 1个月的战士运动后即刻和运动后 1h红细胞压积无明显改变(P <0 .0 5 ) ,而全血SOD 1下降 ,血粘度升高 ,和运动前比较有显著差异 (P <0 .0 5～ 0 .0 1)。结论 :提示进入高原人血粘度增高除红细胞增多原因外 ,尚有氧自由基反应的参与。     

Exercise-induced oxidative stress and muscle performance in healthy women: role of vitamin E supplementation and endogenous oestradiol

The purpose of this study was to investigate the individual and combined antioxidant effects of menstrual cycle phase-related alterations in blood serum oestradiol concentrations and of dietary vitamin E supplementation on exercise-induced oxidative stress and muscle performance. A group of 18 sedentary women, aged 19–35 years, were given supplements of 300 mg α-tocopherol (n=10) or placebo (n=8) daily during the course of two menstrual cycles. The subjects exercised the knee isokinetically to exhaustion after cycling submaximally at 50% maximal oxygen uptake during the menstrual and preovulatory phases of their menstrual cycles. Blood samples were taken before and after the exercise, to evaluate haematocrit, plasma lactic acid and malondialdehyde concentrations, erythrocyte antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and apolipoprotein B containing lipoprotein (non-high density lipoprotein, HDL, fraction) oxidation. Serum vitamin E, follicle stimulating hormone, luteinizing hormone and oestradiol concentrations were measured in pre-exercise blood samples. Neither vitamin E supplementation nor oestradiol concentrations influenced SOD and GPx activities or the susceptibility of the non-HDL fraction to oxidation while at rest. Plasma malondialdehyde concentration was unaffected by exercise, however significant reductions in erythrocyte SOD and GPx activities and increased susceptibility of the non-HDL fraction to oxidation were noted after exercise. Exercise-induced changes were reduced when oestradiol concentration was high in the preovulatory phase, independent of the serum vitamin E concentrations. In addition, both pre- (r=0.58, P < 0.05) and post-exercise (r=0.73, P < 0.001) GPx activities in placebo administered subjects were positively correlated with oestradiol concentrations. In conclusion, these findings suggest a better protective role of oestradiol against oxidative injury, compared to vitamin E. Exhausting muscle performance was, however, not influenced by vitamin E supplementation and/or cycle-phase related changes in oestradiol concentrations. Accepted: 18 September 2000     

小鼠创伤性休克时血中糖,乳酸和NPN变化的发生

小鼠创伤性休克时血中糖，乳酸和ＮＰＮ升高。休克９０ｍｉｎ血糖开始回降，１２０ｍｉｎ骤降而成为死亡的先兆。６５４－２和ＡＬ可预防高乳酸血，对高氮质血无效，因为过多的含氮物主要来自破坏的组织而非代谢障碍。６５４－２可使高血糖曲线右移，延长存活时间，ＡＬ无此作用。除肾外，心，肝，肺均有ＭＤＡ升高；６５４－２可预防心，肝的ＭＤＡ升高而对肺无效；ＡＬ可预防肺，肝ＭＤＡ升高而对心无效；提示不同器官的自由基来源     

胱抑素C与肾动态显像联合检查在肾功能员害时的临床意义

目的探讨胱抑素C（Cys C）与肾动态显像在肾功能损害时的临床意义。方法对52例肾脏病患者均行肾动态显像、血清Cys C和肌酐（Cr）检测分析。结果血清Cys C浓度随着肾功能损害程度的增加而上升,肾动态显像随着肾功能损害程度的增加而下降,均能准确、直观地了解肾功能损害程度。结论 Cys C与肾动态显像联合检查可以更加合理的了解肾小球滤过率的变化,是评估肾功能损伤程度的可靠指标。