脾虚三证模型大鼠脂质过氧化损伤的比较

目的：探讨实验性脾虚大鼠脂质过氧化损伤的差异性,方法：采用饮食加劳倦等 合因素分别复制脾虚不同主型动物模型,观察各模型组和治疗组的脂质过氧化物（LPO）的含量和谷胱甘肽过氧化物酶（GSH－Px) ,超氧化物歧化酶（SOD）,心肌黄酶（DTD）活性变化。结果,各脾虚模型大鼠LPO呈不同程度升高,各种抗氧化酶活性不同程度下降,且且间差异显著,各治疗组药物具有降低LPO,升高抗氧化酶活性的作用,结论：脂质过氧化损伤是脾虚三证的共同症理生理基础。     

脾虚三证模型大鼠脂质过氧化损伤的比较

探讨实验性脾虚大鼠脂质过氧化损伤的差异性。方法采用饮食加劳倦等复合因素分别复制脾虚不同证型动物模型。观察各模型组和治疗组的脂质过氧化物(LPO)的含量和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物岐化酶(SOD)、心肌黄酶(DTD)的活性变化。结果各脾虚模型大鼠LPO呈不同程度升高,各种抗氧化酶活性不同程度下降,且组间差异显著。各治疗组药物具有降低LPO、升高抗氧化酶活性的作用。结论脂质过氧化损伤是脾虚三证的共同病理生理基础。     

大黄泻下与劳倦过度单、复因素造模脾虚小鼠过氧化与抗氧化改变的比较研究

目的：探讨单因素与复合因素造模法对脾虚动物模型生物膜结构和功能改变的规律及其机制。方法：70只小白鼠随机分为4组,即大黄泻下造模（A）组20只,劳倦过度造模（C）组20只,大黄泻上加劳倦过度造模（AC）组20只,空白对照（O）组10只。观察各组小白鼠丙二醛（MDA）、共轭双烯（CD）、过氧化氢酶（Cat)、超氧化物歧化酶（SOD）及过氧化物酶（GSH－Px）的变化,结果：3种方法塑造的脾虚小鼠模型均出现了体重下降,MDA、CD升高,Cat,SO,GSH-Px下降,且脂质过氧化损伤程度和抗氧化氧化酶活性下降程度以AC组为最重。结论：脾虚造模方法以大黄泻下加劳倦过度法为优,复因素脾虚造模法要优于单因素脾虚造模法。     

3种脾虚证模型大鼠胃黏膜损伤情况的比较

[目的]比较3种不同造模方法所致脾虚证模型大鼠胃黏膜损伤情况.[方法]将40只大鼠随机分成5组,即空白1组(5只),空白2组(5只)、利血平组(10只)、甘蓝猪油组(10只)、小承气组(10只).造模过程观察动物一般情况,包括毛发光泽度,活动、反应、大便、食量,体重.光镜下观察胃黏膜的病理组织学变化.[结果]3种造模方法均能使大鼠出现类似临床脾虚证的表现,在光镜下观察符合胃底、胃窦部黏膜糜烂的表现.其中2周后观察,与甘蓝猪油组比较,小承气组黏膜缺损较重,利血平组黏膜下水肿较重.小承气组实验6周后表现较2周、4周加重.[结论]结合一般情况及光镜下结果评价,小承气组造模方法较好.     

NO和脂质过氧化与老年矽肺关系的研究

目的　探讨ＮＯ和脂质过氧化与老年矽肺的关系。方法　检测８５ 例老年矽肺患者和８０ 例健康老年人的血浆ＮＯ（Ｐ－ＮＯ）、过氧化脂质（Ｐ－ＬＰＯ）及红细胞超氧化物歧化酶（Ｅ－ＳＯＤ）、过氧化氢酶（Ｅ－ＣＡＴ）、谷胱甘肽过氧化物酶（Ｅ－ＧＳＨ－Ｐｘ）、过氧化脂质（Ｅ－ＬＰＯ）值。结果　与对照组比较,患者组Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ 均值显著降低,Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ 均值显著升高（Ｐ＜ ０．００１）;直线回归和相关分析表明上述各检测值与患者病程均有相关;逐步回归表明患者病情、肺功能状态与Ｐ－ＮＯ、Ｅ－ＳＯＤ、Ｅ－ＬＰＯ 值相关最密切。结论　矽肺患者体内ＮＯ 代谢异常,氧化抗氧化平衡严重失调,氧化和脂质过氧化反应病理性加剧。     

大鼠睾丸衰老及脂质过氧化

目的　探讨睾丸衰老程度与因氧自由基导致脂质过氧化的关系。方法　对老年组与非老年组大鼠睾丸组织进行 L PO含量和 SOD活力测定 ,同时取病理切片在光镜及电镜下观察组织学改变 ,并分别做血睾酮及雌二醇浓度测定 ,分析睾丸衰老与脂质过氧化的关系。结果　血睾酮浓度老年组较非老年组明显降低 (P<0 .0 1 ) ;血雌二醇浓度老年组较非老年组明显升高 (P<0 .0 1 )。睾丸组织病理切片在光镜及电镜下观察均表现随增龄衰老明显。睾丸组织 LPO含量老年组较非老年组明显升高 (P<0 .0 1 ) ;SOD活力老年组较非老年组明显降低 (P<0 .0 1 )。结论　大鼠睾丸组织脂质过氧化水平与其衰老程度相关 ,随着增龄 ,脂质过氧化损伤增强 ,衰老加重。     

3种脾虚小鼠红细胞膜流动性变化的研究

目的：研究几种脾虚证模型小鼠红细胞（RBC）模流动性（LFU）的变化规律。方法：分别用大黄、番泻叶、利血平制作脾虚模型。用血细胞分析仪检测不同模型小鼠血常规指标的变化，用荧光偏振法检测不同模型小鼠RBC LFU和微粘度（η）的变化。结果：不同造模方法对小鼠血常规指标，除平均血细胞容积外并无明显影响，但均使3种模型小鼠RBV LFU降低，η增加，结论：RBC LFU有可能成为评价脾虚证的一个客观指标。     

Melatonin Reduces Quinolinic Acid-Induced Lipid Peroxidation in Rat Brain Homogenate

The protective effects of melatonin against the neurotoxin, quinolinic acid, were investigated in rat brain homogenate using the thiobarbituric acid assay. Quinolinic acid increased lipid peroxidation in a dose dependent manner. When homogenate was co-treated with melatonin there was a significant decrease in lipid peroxidation. The results of the present report show that melatonin may play a protective role in the brain against the neurohormone quinolinic acid, which has been identified as a causative agent in Huntington's Disease.     

氟对发育中大鼠脑脂质过氧化作用的影响

给孕期及哺乳期母鼠自由饮用0.6,5,25mg/L 含氟水,观察所生仔鼠21天龄对脑脂质过氧化作用。结果显示,氟可降低脑超氧化物歧化酶(SOD)的活性,增加脑谷胱甘肽(GSH)消耗,但脂质过氧化代谢产物丙二醛(MDA)未显著增加。     

Striatal Metabolism of Hexanal,a Lipid Peroxidation Product,in the Rat

Free radical induced lipid peroxidation may play a role in neurodegeneration and peroxidation leads to the formation of hexanal from -6 fatty acids. We have previously demonstrated in vitro that pyruvate dehydrogenase (PDH) catalyzes the condensation of saturated aldehydes with pyruvate to form acyloins. We have further shown in perfused rat heart that hexanal, presumably via PDH, is converted to 3-hydroxyoctan-2-one and that it in turn can be reduced to 2,3-octanediol. We now extend this work using intra-striatal microdialysis to show that this reaction also occurs in rat brain. The reduction of hexanal to hexanol was also evaluated. Microdialysis probes were implanted bilaterally in the striatum and were infused with hexanal with and in the absence of added pyruvate. Analysis of microdialysis samples showed a release of 3-hydroxyoctan-2-one (9.5-10.5 pmol/min), 2,3-octanediol (2.2-2.7 pmol/min) and hexanol (64-74 pmol/min). Pyruvate addition did not increase 3-hydroxyoctan-2-one or 2,3-octanediol production. In a second series of experiments where no exogenous hexanal was infused, endogenous production of 3-hydroxyoctan-2-one (1.0-1.3 pmol/min) and 2,3-octanediol (1.0-1.2 pmol/min) was still observed, although no hexanol was detected. We also investigated the possibility that oxidative stress induced by 1-methyl-4-phenylpyridinium (MPP⁺) would increase lipid peroxidation resulting in increased production of 3-hydroxyoctan-2-one. Analysis of samples collected following MPP⁺ infusion indicated no additional increase suggesting that brief exposure to MPP⁺ does not increase hexanal formation over baseline levels during the experimental period.     

番泻叶致脾虚证动物模型的造型方法

为探讨建立脾虚证动物模型的方法，采用番泻叶水浸剂灌服大白鼠，结果实验组大鼠均出现了泄泻、食少、消瘦、体重减轻、神志萎靡、四肢不收、毛色枯槁、蜷缩聚堆等症状，且易疲劳，游泳耐力降低。认为灌服番泻叶水浸剂可造脾虚证大鼠模型，且定量准确，简单易行。     

Cyanide-Induced Free Radical Production and Lipid Peroxidation in Rat Brain Homogenate is Reduced by Aspirin

The neuroprotective properties of aspirin were investigated using cyanide-induced neurotoxicity as model. Cyanide, a known neurotoxic agent significantly increased lipid peroxidation and superoxide anion levels in rat brain homogenate in a concentration-dependent manner (0.25-1.0 mM). When homogenate, containing 1.0 mM KCN was co-treated with aspirin (1.0 mM) there was a significant decrease in lipid peroxidation. Aspirin (0.5 mM and 1.0 mM) also significantly reduced KCN-induced superoxide anion generation. The results of the present report therefore indicate a neuroprotective role for aspirin.     

Indomethacin Reduces Lipid Peroxidation in Rat Brain Homogenate by Binding Fe2+

One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. Since non steroidal anti-inflammatory drugs (NSAIDS) have been shown to reduce the severity of AD, we investigated the possible mechanism by which indomethacin could afford neuroprotection. Our results show that indomethacin (1 mM) is able to reduce the iron-induced rise in lipid peroxidation in rat brain homogenates. In addition, our NMR data indicate that indomethacin binds the Fe²⁺/Fe³⁺ ion. This was confirmed by a study using UV/Vis spectrophotometry. The results imply that indomethacin provides a neuroprotective effect by binding to iron and thus making it unavailable for free radical production.     

Stimulation of Lipid Peroxidation in Vitro in Rat Brain by the Metabolites Accumulating in Maple Syrup Urine Disease

In this study we investigated the in vitro effects of the metabolites accumulating in maple syrup urine disease on lipid peroxidation in brain of young rats. Chemiluminescence and thiobarbituric acid-reactive substances were measured in brain homogenates from 7- and 30-day-old rats in the presence of 10 mM of the branched-chain amino acids L-leucine, L-isoleucine, or L-valine; their keto acids L-2-ketoisocaproic acid, L-2-keto-3-methylvaleric acid, or L-2-ketoisovaleric acid; or the hydroxy derivatives L-2-hydroxyisocaproic acid, L-2-hydroxy-3-methylvaleric acid, or L-2-hydroxyisovaleric acid separately added to the incubation medium. We observed that all amino acids, keto acids, and hydroxy acids accumulating in this disease stimulate to a variable degree the in vitro parameters of lipid peroxidation tested in homogenates of rat brain. The results indicate a possible participation of oxidative stress in the neuropathology of maple syrup urine disease patients, especially during a crisis, when the metabolites are highly increased, and point to the use of antioxidant drugs as a possible adjuvant therapy in such situations to improve the neurological status of the patients and to prevent sequelae.