褪黑素对苯妥英诱发胚胎脑组织氧化性损伤的拮抗作用

目的　研究褪黑素 (MT)对苯妥英 (Phe)诱发的胚胎脑组织氧化性损伤有无保护作用。方法　妊娠Wistar母鼠于妊娠 (GD11～ 14 )ig 0和 10 0mg·kg- 1Phe ,4 0mg·kg- 1MT及 4 0mg·kg- 1MT +10 0mg·kg- 1Phe ;GD15脱颈椎处死动物 ,测定胎鼠脑组织各种与氧化性损伤有关的指标。结果　妊娠期染毒Phe导致胚胎脑组织H2 O2 水平升高 ,脂质过氧化和蛋白质氧化产物增加 ,超氧化物岐化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性下降 ,总还原型谷胱甘肽(GSH)含量及总抗氧化力降低。妊娠期MT处理减少正常胎鼠脑中H2 O2 及产率 ;同时MT和Phe共同处理可阻断Phe诱发的氧化性损伤 ,GSH耗竭和抗氧化酶活性的下降。结论　MT对Phe诱发的胎鼠脑组织氧化性损伤有一定的拮抗作用。     

云芝多糖对小鼠心、肝、脾、肾和红细胞抗氧化能力的影响

通过测定小鼠心、肝、脾、肾组织和红细胞脂质过氧化物含量和硒谷胱甘肽过氧化物酶活性，观察了云芝多糖对机体各组织及红细胞抗氧化能力的影响。结果表明，云芝多糖能提高机体各组织的硒谷胱甘肽过氧化物酶活性及降低脂质过氧化物含量，提示云芝多糖能有效地提高机体抗氧化能力，为防止或减轻脂质过氧化损伤提供了实验依据。     

硫酸酯化虎奶多糖的制备及其抗氧化作用研究

目的对虎奶多糖进行硫酸酯化修饰 ,并研究其抗氧化活性。方法用氯磺酸 吡啶法对虎奶多糖进行硫酸酯化修饰得到硫酸酯化虎奶多糖 (S HNP) ;以Fe2 + Vc为氧自由基生成系统 ,体外观察S HNP对·OH引起的大鼠肝线粒体脂质过氧化损伤的保护作用 ;用化学发光法研究化学模拟体系CuSO4 Phen Vc H2 O2 DNA中S HNP对DNA损伤的保护作用 ;连苯三酚自氧化法观察S HNP对O·- 2 的清除作用。结果S HNP能显著抑制·OH引起的线粒体脂质过氧化产物TBARS的生成、线粒体的肿胀及膜流动性的降低 ;对·OH导致的DNA损伤有一定保护作用 ;对O·-2 有直接清除作用。结论S HNP具有较强的抗氧化活性。     

何首乌多糖对氧自由基及抗氧化酶活性的作用研究

目的:研究何首乌多糖对氧自由基及抗氧化酶活性的作用及其机制.方法:用D-半乳糖注射小鼠致亚急性衰老模型,同时何首乌多糖50或150 mg·kg·d-1)连续灌胃8周,观察其对模型小鼠体内脂质过氧化产物及抗氧化酶活性的影响.结果:50或150 mg·kg-1·d-1)何首乌多糖能使模型小鼠血清和肝、肾组织中SOD,肝、肾组织中GSH-PX酶活力明显上升;血清、肝、肾组织中MDA及脑组织中LF明显下降.结论:何首乌多糖可显著提高模型小鼠体内抗氧化酶活性,清除氧自由基及抑制脂质过氧化.     

水溶性山药多糖对小鼠的抗衰老作用

经提取、分离纯化,制备山药多糖精品;并通过腹腔注射山药多糖精品,考察其对小鼠的抗衰老作用。实验结果显示,给药组小鼠体内谷胱甘肽过氧化物酶、过氧化氢酶、超氧化物歧化酶和脑Ｎａ＋／Ｋ＋－ＡＴＰ酶活性均增加;单 氧化酶Ｂ活性及过氧化脂质和脂褐质含量均降低。     

羊栖菜多糖对氧化应激人成纤维细胞的保护作用

目的研究羊栖菜多糖对氧化应激的人皮肤成纤维细胞的保护作用及机制。方法以0.8 mmol/L H2O2诱导人皮肤成纤维细胞建立氧化应激模型,MTT法测定不同浓度羊栖菜多糖(15、30、60mg/L)对过氧化氢(H2O2)损伤人皮肤成纤维细胞增殖的影响,Hoechst 33258染色法观察细胞凋亡,流式细胞仪测定细胞周期分布。测定细胞丙二醛(MDA)含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性、还原性谷胱甘肽(GSH)水平和活性氧(ROS)水平。结果羊栖菜多糖可抑制H2O2对人皮肤成纤维细胞增殖活性的下降和凋亡率的上升,维持细胞正常形态。流式细胞仪检测表明,羊栖菜多糖能显著降低H2O2损伤的细胞G0/G1期阻滞现象;升高SOD和GSH-Px活力,降低MDA和ROS水平,升高GSH水平,差异有统计学意义且具有剂量依赖性(P<0.05,P<0.01)。结论羊栖菜多糖能减轻H2O2对人皮肤成纤维细胞的氧化损伤,具有较好的抗氧化保护作用,与其增强抗氧化酶活性,降低脂质过氧化有关。     

南沙参多糖抗衰老作用的实验研究

目的　探讨南沙参多糖对老龄小鼠及果蝇的抗衰老作用及其机制。方法　考察用药前后老龄小鼠肝、脑脂褐素和单胺氧化酶 ,血中皮质醇、睾酮及超氧化物歧化酶、丙二醛和谷胱甘肽过氧化物酶的改变 ,同时观察药物对果蝇寿命及性活力的影响。结果　 1 0 g·kg-1南沙参多糖降低老龄小鼠肝、脑脂褐素含量 ,显著抑制老龄小鼠血清中丙二醛的生成 ;提高老龄小鼠红细胞中超氧化物歧化酶及全血中谷胱甘肽过氧化物酶的活性 ;可使老龄小鼠肝、脑中B型单胺氧化酶的活性降低。该药可增加老龄小鼠血清中睾酮的含量 ;同时 ,南沙参多糖 10 g·kg-1可延长果蝇的平均寿命和最高寿命 ,提高其性活动能力 ,增加交配频率。结论　南沙参多糖具有抗衰老作用     

中华跌打丸抗氧化实验

研究中华跌打丸的抗氧化作用.将昆明小鼠随机分组,高、中、低剂量组分别经口给予不同浓度(0.16g·ml-1、0.08g·ml-1、0.04g·ml-1)受试样品,空白对照组则给予同体积溶剂,连续给药30天后取血测抗氧化酶活力,次日给受试样品或溶剂1h后,用溴代苯油(0.32g·kg-1)造模致肝损伤,测肝组织抗氧化酶活力和过氧化脂质含量.受试样品高剂量组全血谷胱甘肽过氧化物酶(GSH-Px)活力显著高于空白对照组(p＜0.01);各剂量组血清总超氧化物歧化酶(SOD)活力显著高于空白对照组(p＜0.01).各剂量组肝组织过氧化脂质丙二醛(MDA)的含量显著低于模型对照组(p＜0.01),高、中剂量组肝组织GSH-Px活力显著高于模型对照组(p＜0.01).结果显示中华跌打丸具有一定的抗氧化功能,对肝组织脂质过氧化损伤具有一定保护作用.     

生姜提取物对四氯化碳损伤小鼠肝脏脂质过氧化的影响

目的研究生姜提取物对CCl4损伤小鼠肝脏脂质过氧化的影响。方法分别以高、中、低剂量生姜提取物给小鼠灌胃,6h后经口给予10%的CCl4染毒。观察不同组小鼠肝脏组织抗氧化酶(超氧化物歧化酶SOD、谷胱甘肽过氧化物酶GSH-Px)活性和脂质过氧化产物丙二醛(MDA)含量的变化。结果高剂量姜液组抗氧化酶活性降低,MDA含量升高;低剂量姜液组抗氧化酶活性升高,MDA含量降低。结论中、低剂量的生姜提取物对CCl4造成的小鼠抗氧化系统损伤具有保护作用。     

南沙参多糖对小鼠的抗衰老及清除氧自由基作用研究

目的:探讨南沙参多糖对老龄小鼠的抗衰老作用及清除氧自由基作用.方法:考察用药前后老龄小鼠肝、脑脂褐素、血中皮质醇、睾酮含量和肝、脑中单胺氧化酶活性的变化,以及南沙参多糖对老龄小鼠体内超氧化物歧化酶、丙二醛和谷胱甘肽过氧化物酶和体外直接清除氧自由基的作用.结果:1.0 g·kg-1南沙参多糖明显降低老龄小鼠肝、脑脂褐素含量,并增加老龄小鼠血清中睾酮的含量,同时可使老龄小鼠肝、脑中B型单胺氧化酶的活性降低.这些效应与其抑制老龄小鼠血清中丙二醛的生成、提高其红细胞中超氧化物歧化酶及全血中谷胱甘肽过氧化物酶的活性和直接清除体外氧自由基关系密切.结论:南沙参多糖对于老龄小鼠有明显的抗衰老效应.     

Protective effects of curcumin against ischaemia/reperfusion insult in rat forebrain.

Oxidative stress is believed to be implicated in the pathogenesis of postischaemic cerebral injury. Many antioxidants were shown to be neuroprotective in experimental models of cerebral ischaemia/reperfusion (I/R). The present study was designed to investigate the potential protective effects of curcumin (CUR) against I/R insult in rat forebrain. The model adopted was that of surgically-induced forebrain ischaemia, performed by means of bilateral common carotid artery occlusion (BCCAO) for 1 h, followed by reperfusion for another 1h. The effects of a single i.p. dose of CUR (50, 100 or 200 mg kg(-1)), administered 0.5 h after the onset of ischaemia, were investigated by assessing oxidative stress-related biochemical parameters in rat forebrain. CUR, at the highest dose level (200 mg kg(-1)), decreased the I/R-induced elevated xanthine oxidase (XO) activity, superoxide anion (O(2)*(-)) production, malondialdehyde (MDA) level and glutathione peroxidase (GPx), superoxide dismutase (SOD), and lactate dehydrogenase (LDH) activities. On the other hand, CUR did not affect the declined reduced glutathione (GSH) content due to I/R insult. Worth mentioning is that the activity of catalase (CAT) did not change in response to either I/R insult or drug treatment. In conclusion, CUR was found to protect rat forebrain against I/R insult. These protective effects may be attributed to its antioxidant properties and/or its inhibitory effects on xanthine dehydrogenase/xanthine oxidase (XD/XO) conversion and resultant O(2)*(-) production.     

钙通道阻滞剂抗肝缺血—再灌注损伤作用机制的实验研究

目的 探讨钙通道阻滞剂（ＣＣＥＢ）对肝缺血一再灌注损伤（ＨＩＲＩ）防治作用的机制。方法制备家兔ＨＩＲＩ模型,动态观察维拉帕米（ＶＰ）和地尔硫卓（ＤＴ）对肝组织及血中黄嘌呤氧化酶（ＸＯ）、超氧化物歧化酶（ＳＯＤ）活性及脂质过氧化物（ＬＰＯ）浓度的影响。结果 ＶＰ组和ＤＴ组ＯＸ活性及ＭＤＡ含量分别显著低于对照组（均Ｐ＜０．０１）,而ＳＯＤ活性与对照组比较均无显著性差异（均 Ｐ＞ ０．０５）。结论 ＣＣＥＢ抗 ＨＩＲＩ的机制与其降低 ＸＯ活性、抑制脂质过氧化反应密切相关。     

Brain regional responses in antioxidant system to alpha-lipoic acid in arsenic intoxicated rat

Impaired antioxidant defense mechanisms and oxidative stress are implicated in the pathogenesis of arsenic toxicity. Our study was designed to determine whether alpha-lipoic acid, which has been shown to have substantial antioxidant properties, when administered (70 mg/kg body weight) once daily for 60 days along with arsenic (100 ppm sodium arsenite mixed in drinking water) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD-total SOD, Mn SOD, Cu/Zn SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) in rat brain regions such as cortex, hypothalamus, striatum, cerebellum and hippocampus. The present study also examined the effect of alpha-lipoic acid over arsenic-induced oxidant production and lipid peroxidation level (LPO) in discrete brain regions of rats. The cortex, striatum and hippocampus showed greater decreases in GSH-Px enzyme activity than cerebellum and hypothalamus with arsenic exposure. Striatum had the greatest percentage of decreased activities of total SOD and Mn SOD, whereas cortex had the greatest percentage decrease in the activity of Cu/Zn SOD in arsenic-alone treated rats. Hypothalamus and cerebellum exhibited the lowest catalase activity among all tested regions in arsenic-only treated rats. Rate of dichlorofluorescin oxidation, an indication of reactive oxygen species and other intracellular oxidants production was increased with arsenic exposure in all brain regions studied. Cortex, hippocampus and striatum exhibited greater increase of LPO levels than cerebellum and hypothalamus. SOD, CAT, GSH-Px activities were upregulated in arsenic plus lipoic acid treated versus arsenic-only treated rats. Also, simultaneous lipoic acid treatment along with arsenic proved to be sufficient in reducing oxidant production and LPO level in all rat brain regions. Our results demonstrate that arsenic-induced deficits in antioxidant enzyme activities and increase in oxidant production and lipid peroxidation level in brain regions can be overcome through simultaneous treatment with lipoic acid.     

川芎嗪对围术期肝脏缺血—再灌注损伤的防治作用

目的：探讨川芎嗪对围术期肝脏缺血－再灌注损伤（ＨＩＲＩ）的防治作用。方法：观察１８例肝癌患者手术过程中血中ＧＰＴ、ＳＯＤ、ＧＳＨ－ＰＸ、ＸＯ活性及ＭＤＡ含量的动态变化及川芎嗪的影响。结果：川芎嗪组与对照组比较,ＳＯＤ和ＧＸＨ－ＰＸ活性明显增高（Ｐ〈０．０５和Ｐ〈０．０１）,ＭＤＡ含量及ＧＰＴ值显著下降（均Ｐ〈０．０１）。结论：川芎秦上脏围术期ＨＩＲＩ有明显的防护作用。     

Protective effects of L-arginine on pulmonary oxidative stress and antioxidant defenses during exhaustive exercise in rats

AIM: To assess the effects of L-arginine (L-Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. METHODS: Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L-Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2% L-Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione (GSH)] were investigated in this study. RESULTS: L-Arg supplementation significantly reduced exercise-induced elevations of XO and MPO activities in lung. L-Arg reversed the exercise-induced increase in SOD and GR activities, but increased CAT and GPX activities. L-Arg administration also significantly increased the GSH levels in plasma. CONCLUSION: L-Arg supplementation can prevent elevations of XO and MPO activities in the lung and favorably influence pulmonary antioxidant defense systems after exhaustive exercise.     

褪黑素对脑缺血再灌注后脑内抗氧化酶及MDA的影响

目的　研究褪黑素 (melatonin ,MT)对脑缺血再灌注沙土鼠脑组织谷胱甘肽过氧化物酶 (GPx)、超氧化物歧化酶(SOD)活性及丙二醛 (MDA)含量的影响 ,探讨MT的脑保护作用机制。方法　采用沙土鼠双侧颈总动脉结扎法制作前脑缺血再灌注损伤的模型 ,缺血前 30min腹腔注射MT ,测定脑缺血再灌注 1h沙土鼠大脑皮层和纹状体GPx、SOD活性及MDA含量。结果　脑缺血再灌注后大脑皮层和纹状体GPx、SOD活性降低 ,MDA含量升高 ;MT预处理能部分反转这种变化。结论　MT对脑缺血再灌注损伤有保护作用 ,其机制可能与保护GPx、SOD活性 ,减少脂质过氧化有关     

羊栖菜多糖对L_(615)小鼠LPO含量及GR、GSH—PX、CAT和SOD活性的影向

本文报道了羊栖菜多糖(SFPS)对L_(615)小鼠全血及肝脾脂质过氧化物(LPO)含量以及对各胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GSH—PX)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)等酶活性的影响。结果表明,SFPS可显著降低L_(615)小鼠全血及肝脾LPO的含量,增加CAT、SOD的酶活性,提示SFPS具有清除L_(615)小鼠体内自由基,抗脂质过氧化作用。本文结果提示,SFPS的这些作用可能是其抗白血病作用的机理之一。     

The influence of cytaphate on the status of oxidative metabolism in rats with diabetic nephropathy

The antioxidant effect of cytaphate (0,0-dimethyl-N-cytisinyl phosphate) has been studied in outbred white rats with alloxan-induced insulin-dependent diabetes mellitus. The content of malonic dialdehyde, diene conjugates, ketodienes, middle-weight molecules, primary and secondary products of lipid peroxidation (LPO), and Schiff bases and the activity of catalase, glutathione peroxidase, and adenosine deaminase in erytrocytes have been evaluated. The state of oxidative protein modification, the content of malonic dialdehyde and diene conjugates, and the superoxide-anion production in the blood plasma have been determined. In the blood of animals with model diabetes, the LPO and oxidative protein modification processes were intensified and the level of superoxide anion production was increased. The administration of cytaphate led to a decrease of the LPO intensity and oxidative protein modification and to normalization of the level of superoxide anion production and the activity of enzymes involved in the antioxidant protection system.     

脱氢表雄酮硫酸酯对体外大鼠脑皮层神经细胞拟老化反应的影响

用原代培养Wistar大鼠胎鼠脑皮层神经细胞,从形态学和生化学方面研究自由基、无血清培养对神经元的损伤以及脱氢表雄酮硫酸酯(DHEAS)的保护作用。结果显示,神经细胞与自由基作用及在无血清培养条件下,细胞生存率明显下降,培养液的上清液中乳酸脱氢酶(LDH)活性显著提高,丙二醛(MDA)含量明显增加,超氧物岐化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力显著下降。相差显微镜下观察,神经细胞突起回缩,颗粒增加,折光性下降。DHEAS剂量依赖地提高神经细胞损伤后细胞生存率,降低LDH的释放及MDA的生成,并显著提高抗氧化酶活性。结果提示,DHEAS可能通过抑制脂质过氧化物生成及提高抗氧化酶活性来保护拟衰老反应中的大脑皮层神经细胞。     

1,6-二磷酸果糖对阿霉素导致大鼠心肌细胞凋亡的影响

目的　研究 1,6 二磷酸果糖 (FDP)对阿霉素 (ADM )导致大鼠心肌细胞凋亡的影响。方法　给大鼠腹腔注射ADM ( 2 5 0mg·kg-1,隔日 1次 ,共 6次 )处理大鼠 ;给ADM处理的大鼠腹腔注射不同剂量的FDP(隔日 1次 ,共 2 1次 )进行干预。分别用TBA法、硝酸还原酶法、DTNB法、邻苯三酚自氧化法测定心肌的脂质过氧化物 (LPO)含量、一氧化氮 (NO)含量、谷胱甘肽过氧化物酶 (GPx)活性、超氧化物歧化酶 (SOD)活性 ;用透射电镜技术和TUNEL法检测心肌细胞凋亡 ;用原位杂交法检测心肌的诱导型一氧化氮合酶 (iN OS)mRNA表达。结果　FDP( 3 0 0 ,60 0 ,12 0 0mg·kg-1)干预ADM处理的大鼠后 ,均可降低心肌的LPO及NO含量、减少心肌细胞的凋亡数量、降低心肌iNOSmRNA的表达水平、增加心肌的SOD及GPx活性。结论　FDP抑制ADM导致心肌细胞凋亡 ,减轻ADM对心肌的毒性损伤 ,其机制2 0 0 1 0 4 12收稿 ,2 0 0 1 0 5 30修回 广西自然科学基金 (No 982 40 0 1)和广西教育厅科学基金 (No 1999 34 9)资助1 广西肿瘤研究所生化室 ,南宁　 5 30 0 2 1作者简介 :阳冠明 ,男 ,39岁 ,医学硕士 ,副研究员 ,硕士生导师。Tel:0 771 5 35 8130 (O) ,5 35 130 5 (H) ;林善修 ,男 ,67岁 ,教授 ,博士生导师可能与其保护心肌的SOD及GPx活性、抗脂质?