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外源性SOD抗高压氧脂质过氧化作用的实验研究

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中华医学杂志 1991年第11期71卷 642-644页

作者：沈剑刚陈瑗刘子藩侯灿第一军医大学脂质过氧化研究组中山医科大学附属第一医院高压氧科中山医科大学病理生理教研室

为探讨超氧化物歧化酶(SOD)的抗氧毒性作用,我们观察了不同剂量SOD腹腔注射对大鼠在高压氧条件下血液、心脑组织脂质过氧化的抑制作用。一、材料与方法

关键词：超氧化物歧化酶/投药和剂量高压氧脂质过氧化作用/药物作用

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玉屏风多糖对小鼠化学性肝损伤的影响

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安徽医科大学学报 2011年第1期46卷 49-52页

作者：陈方军李俊王佳佳安徽医科大学药学院合肥230032 安庆医药高等专科学校安庆246052

目的观察玉屏风多糖(YPF-P)对D-氨基半乳糖(D-Gal)致化学性肝损伤小鼠血清、肝组织中丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)含量以及TNF-α表达水平的影响,探讨YPF-P对D-Ga... 详细信息

目的观察玉屏风多糖(YPF-P)对D-氨基半乳糖(D-Gal)致化学性肝损伤小鼠血清、肝组织中丙氨酸氨基转移酶(ALT)、天门冬酸氨基转移酶(AST)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)含量以及TNF-α表达水平的影响,探讨YPF-P对D-Gal致小鼠化学性肝损伤的作用机制。方法经预防给药7d后,采用D-Gal复制小鼠肝损伤模型,测定小鼠肝脏指数、血清ALT和AST及肝匀浆中SOD、GSH、MDA含量,免疫组化SP法观察肝细胞中TNF-α表达水平,HE染色观察肝脏病理组织学变化。结果 YPF-P(200mg/kg)能显著降低D-Gal诱导化学性肝损伤小鼠的肝脏指数;降低血清中升高的ALT、AST含量;升高肝匀浆中降低的SOD活性和GSH水平,降低升高的MDA含量;抑制肝细胞中TNF-α表达,减轻小鼠肝脏病理损伤。结论 YPF-P对D-Gal所致小鼠化学性肝损伤具有一定的保护作用,其保护机制可能与抑制脂质过氧化,增强机体抗氧化能力有关。

关键词：肝疾病/化学诱导肿瘤坏死因子-α 脂质过氧化作用/药物作用

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粗叶悬钩子抗肝损伤类活性成分对CCl4损伤大鼠肝细胞的影响

粗叶悬钩子抗肝损伤类活性成分对CCl4损伤大鼠肝细胞的影响

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作者：赵锦燕福建中医学院

学位级别：硕士

目的:通过药效学实验跟踪有效成分,筛选粗叶悬钩子抗肝损伤类的活性成分,对有效成分进行初步鉴定,并对有效成分作用机制作初步的探讨。方法:（1）中药常规提取方法制备粗叶悬钩子分类提取物总生物碱,并进行检测。（2）根据总生物碱内成... 详细信息

目的:通过药效学实验跟踪有效成分,筛选粗叶悬钩子抗肝损伤类的活性成分,对有效成分进行初步鉴定,并对有效成分作用机制作初步的探讨。方法:（1）中药常规提取方法制备粗叶悬钩子分类提取物总生物碱,并进行检测。（2）根据总生物碱内成分极性的不同,分别用乙酸乙酯、正丁醇、氯仿等溶剂萃取其不同极性部位。（3）制备小鼠急性肝损伤模型,并用不同极性部位进行干预,观察效果,选取有效极性部位。（4）通过传统柱层析的方法,进一步分离有效极性部位,并合并极性相同或相近的馏分。（5）通过制备色谱法和高效液相色谱法,进一步分离成分。（6）培养大鼠肝细胞,并制备肝细胞损伤模型,通过药物干预模型,观察相关指标的变化,最终选取粗叶悬钩子抗肝损伤的有效成分。结果:（1）粗叶悬钩子抗肝损伤有效成分-129③的不同药物浓度均可不同程度地降低肝细胞培养上清液中ALT、AST的含量;（2）129③的不同药物浓度能不同程度地升高肝细胞培养上清液中SOD的活性,同时降低MDA的含量;（3）129③的不同药物浓度能不同程度地促进肝细胞的增殖:（4）129③能不同程度地调节细胞生长周期,促使细胞向S期转化;（5）129③能显著下调CCl4损伤的大鼠肝细胞中Caspase-3mRNA的表达,并且上调PCNAmRNA的表达。结论:（1）129③是粗叶悬钩子中抗肝损伤的有效活性成分;（2）129③能保护肝细胞膜,减轻肝细胞受损的程度;（3）129③能抑制自由基的生成和脂质过氧化产物的生成,提高肝细胞的抗氧化能力;（4）129③促进肝细胞地增殖,抑制细胞凋亡;（5）129③能够调节细胞生长周期。

关键词：肝炎,中毒性/中医药疗法蔷薇科/药理学植物提取物/药理学中药化学成分/药理学肝细胞/药物作用细胞凋亡/药物作用细胞增殖/药物作用脂质过氧化作用/药物作用

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益气养阴解毒活血方治疗慢性乙型肝炎的理论与实验研究

益气养阴解毒活血方治疗慢性乙型肝炎的理论与实验研究

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作者：黄争荣福建中医学院

学位级别：硕士

背景：慢性乙型肝炎(CHB)发病率和复发率均较高的常见病，其确切的病因和发病机仍不完全明了。中医药治疗CHB具有一定优势，但临床尚缺乏理想的中药制剂，故探索治疗CHB的有效药物具有重要意义。目的：收集和查阅大量的相关文献资... 详细信息

背景：慢性乙型肝炎(CHB)发病率和复发率均较高的常见病，其确切的病因和发病机仍不完全明了。中医药治疗CHB具有一定优势，但临床尚缺乏理想的中药制剂，故探索治疗CHB的有效药物具有重要意义。目的：收集和查阅大量的相关文献资料，为益气养阴解毒活血法治疗CHB提供理论依据，通过实验研究揭示益气养阴解毒活血方的作用机理和配伍内在关系，以便有效指导临床用药。方法：收集大量古今医学资料，综合中医学各家所论，研究CHB的中医治疗法则。实验研究中将81只小鼠分为6组：正常对照组、模型对照组、联苯双酯治疗组、益气养阴解毒活血方小、中、大剂量组，另取96只小鼠分为7组：正常对照组、模型对照组、全方组、去益气组、去养阴组、去解毒组、去活血组，均以卡介苗和大肠杆菌内毒素复制CHB模型，分别采用对应中药复方灌胃治疗，正常对照组和模型对照组给予同剂量0.9％生理盐水。给药12天后，观察小鼠在体症状及病理组织学变化，检测小鼠血清谷丙转氨酶、肿瘤坏死因子-α、白介素-6及肝组织总蛋白、超氧化物歧化酶、丙二醛、一氧化氮的水平，分析各项指标在实验中的变化意义。结果：该方能显著改善小鼠肝脏的炎症损害，降低异常升高的血清谷丙转氨酶、丙二醛、一氧化氮、白介素-6，调整肿瘤坏死因子-α水平和升高总蛋白、超氧化物歧化酶水平。益气养阴解毒活血方全方组对上述指标的改善强于其各拆方组。结论：正虚、毒侵、阴伤、血瘀是CHB发病发展的基本病变，益气养阴、解毒活福建中医学院2004届硕士学位论文理旦旦旦旦旦些旦旦旦旦鱼旦里旦鱼血是治疗CHB的基本治法。益气养阴解毒活血方具有改善肝功能、保护肝细胞膜、抗过氧化损伤、拮抗肿瘤坏死因子一Q、白介素一6的所致肝损伤作用及调节免疫功能等作用。该方其配伍合理，是治疗CHB的有效方剂。

关键词：肝炎,乙型,慢性/中医药疗法脂质过氧化作用/药物作用补气药/药理学一氧化氮/血液补阴药/药理学肿瘤坏死因子/血液清热解毒药/药理学白细胞介素6/血液活血祛瘀药/药理学鼠肝/药物作用动物 @益气养阴解毒活血方

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加味泽泻汤对实验性高脂血症大鼠血脂代谢及脂质过氧化影响的研究

加味泽泻汤对实验性高脂血症大鼠血脂代谢及脂质过氧化影响的研究

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作者：谭峰福建中医学院

学位级别：硕士

目的:研究加味泽泻汤对实验性高脂血症大鼠血脂代谢及脂质过氧化的影响,对加味泽泻汤的调脂作用进行客观的评价,并对其作用机理进行初步探讨。方法:1.理论研究:从祖国传统医学和现代医学两个方面,系统阐述高脂血症的研究概况。采用文献... 详细信息

目的: 研究加味泽泻汤对实验性高脂血症大鼠血脂代谢及脂质过氧化的影响,对加味泽泻汤的调脂作用进行客观的评价,并对其作用机理进行初步探讨。方法: 1.理论研究:从祖国传统医学和现代医学两个方面,系统阐述高脂血症的研究概况。采用文献整理和分析的方法,详细论述中医学对高脂血症的病因病机、辨证论治的认识,回顾了近年来现代医学研究高脂血症的进展。结合传统理论及现代药理学研究成果,对加味泽泻汤的方证关系及方病关系进行分析。 2.实验研究:采用高脂乳剂灌胃造成高脂血症大鼠模型,口服给药3周后,腹主动脉采血,测血脂六项、血清超氧化歧化酶（SOD）、血清丙二醛（MDA）,并计算肝脏系数。采用病理学检测方法,观察实验动物肝脏组织形态学的改变。结果: 1.理论研究显示高脂血症主要病因病机为饮食不节,脾胃受损;年老体弱,脏气虚衰;情志内伤,脏腑失调;痰浊瘀血,阻碍气机等。本病与五脏相关,病变中心在脾。根据本病的演变、导师临床经验及现代研究结果,我们认为,痰浊、瘀血为本病的关键,脾虚是本病的基本病机,提出利水健脾,活血消积的治法。并以《金匮》泽泻汤为基础重新组方而成的加味泽泻汤治疗高脂血症属痰阻瘀滞,脾失健运证者。 2.加味泽泻汤能够明显降低高脂血症大鼠血清总胆固醇（TC）,甘油三酯（TG）,低密度脂蛋白（LDL-C）含量,载脂蛋白apoB100,MDA,升高大鼠血清HDL-C,apoA1、SOD水平;肝脏指数明显降低,同时肝脏病理观察结果显示,加味泽泻汤并减轻高脂血症大鼠肝损伤,能明显减轻肝脏脂质沉积。结论: 1.理论研究表明,加味泽泻汤组方符合“方证相合”的配伍理念及“病证相参”的研究思路,具有利水健脾,活血消积的功效,可用于高脂血症中证属痰阻瘀滞,脾失健运者的治疗。 2.实验研究表明,加味泽泻汤能够明显纠正高脂血症大鼠脂质代谢紊乱,降低血清TG、TC、LDL—C含量;具有抗脂质过氧化作用,通过提高抗氧化酶活性、降低脂质过氧化产物含量;保护肝脏组织,减少肝脏脂质沉积,减轻肝细胞脂肪变牲,防治高脂血症,预防脂肪肝的形成。

关键词：高脂血症/中药疗法脂质过氧化作用/药物作用超氧化物歧化酶/血液丙二醛/血液脂蛋白类/血液 @加味泽泻汤

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Nitric oxide inhibition of free radical-mediated cholesterol peroxidation in liposomal membranes

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BIOCHEMISTRY 2000年第23期39卷 6918-6928页

作者： Korytowski, W Zareba, M Girotti, AW Med Coll Wisconsin Dept Biochem Milwaukee WI 53226 USA Jagiellonian Univ Inst Mol Biol Krakow Poland

The ability of nitric oxide ((NO)-N-.) to inhibit propagative lipid peroxidation was investigated using unilamellar liposomes (LUVs) constituted with egg phosphatidylcholine (PC) or 1-palmitoyl-2-oleoylphosphatidylcholine (POPC), [C-14]cholesterol (Ch), and a nonregenerable singlet oxygen-derived primer, 5 alpha-hydroperoxycholesterol (5 alpha-OOH). Exposing LUVs to ascorbate and a lipophilic iron chelate at 37 degrees C resulted in an exponential decay of 5 alpha-OOH and accumulation of free radical-derived 7 alpha- and 7 beta-hydroperoxycholesterol (7 alpha beta-OOH), as detected by high-performance liquid chromatography with electrochemical detection. Thiobarbituric acid-reactive species (TBARS) were generated concurrently in egg PC-containing LUVs. Including the (NO)-N-. donor spermine NONOate (SPNO, 5-50 mu M) or S-nitroso-N-acetyl-D,L-penicillamine (SNAP, 50-100 mu M) in the reaction mixture had no effect on 5 alpha-OOH decay (suggesting that iron was not redox-inhibited) but slowed TEARS and 7 alpha beta-OOH accumulation in a strongly dose-dependent fashion. Decomposed SPNO or SNAP had no such effects, implying that (NO)-N-. was the responsible agent. Accumulation of several [C-14]Ch oxidation products, detected by high-performance thin-layer chromatography with phosphorimaging, was similarly diminished by active SPNO or SNAP. Concomitantly, a new band referred to as RCh.4 appeared, the radioactivity of which increased as a function of incubation time and (NO)-N-. donor concentration. RCh.4 material was also generated via direct iron/ascorbate reduction of 7 alpha-OOH in the presence of (NO)-N-., consistent with 7 alpha-nitrite (7 alpha-ONO) identity. However, various other lines of evidence suggest that RCh.4 is not 7 alpha-ONO, but rather 5 alpha-hydroxycholesterol (5 alpha-OH) generated by reduction of 5 alpha-ONO arising from 7 alpha-ONO rearrangement. 5 alpha-OH was only detected when (NO)-N-. was present in the reaction system, thus providing indirect e

关键词：抗氧化剂/药理学抗坏血酸/药理学胆固醇/类似物和衍生物胆固醇/代谢胆固醇/药理学色谱法高压液相色谱法薄层自由基/代谢动力学脂质过氧化作用/药物作用脂质体/代谢分子结构一氧化氮/药理学亚硝基化合物/代谢过氧化物/代谢过氧化物/药理学磷脂类/代谢硫巴比妥酸反应物/分析

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Effect of n-3 polyunsaturated fatty acid supplementation on lipid peroxidation of rat organs

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LIPIDS 2000年第4期35卷 401-407页

作者： Ando, K Nagata, K Yoshida, R Kikugawa, K Suzuki, M Tokyo Univ Pharm & Life Sci Sch Pharm Hachioji Tokyo 1920392 Japan Kyushu Univ Adv Sci & Technol Res Ctr Fukuoka 8168580 Japan

The present study was undertaken in order to reexamine the effect of n-3 polyunsaturated fatty acid (PUFA)-rich diet supplementation on lipid peroxidation and vitamin E status of rat organs. Male Wistar rats were fed a diet containing safflower or fish oil at 50 g/kg diet and an equal amount of vitamin E at 59 mg/kg diet (1.18 g/kg oil;and 1.5 g/kg PUFA in safflower oil diet, and 4.3 g/kg PUFA in fish oil diet) for 6 wk. Fatty acid composition of total lipids of brain, liver, heart, and lung of rats fed fish oil was rich in n-3 PUFA, whereas that of each organ of rats fed safflower oil was rich in n-6 PUFA. The vitamin E levels in liver, stomach, and testis of the fish oil diet group were slightly lower than those of the safflower oil diet group, but the levels in brain, heart, lung, kidney, and spleen were not different between the two diet groups. The levels of phospholipid hydroperoxides were determined by the high-performance liquid chromatography-chemiluminescence method and the levels of thiobarbituric acid-reactive substances (TBARS) were deter mined at pH 3.5 in the presence of butylated hydroxytoluene with or without EDTA. Levels of phospholipid hydroperoxides and TBARS in the brain, liver, heart, lung, kidney, spleen, stomach and testis of the fish oil diet group were similar to those of the safflower oil diet group. The results indicate that high fish oil intake does not induce increased levels of phospholipid hydroperoxides and TBARS in rat organs.

关键词：丁羟甲苯/药理学色谱法高压液相膳食脂肪类不饱和/投药和剂量膳食脂肪类不饱和/药理学依地酸/药理学脂肪酸类 ω3/投药和剂量脂肪酸类 ω3/药理学鱼油/投药和剂量过氧化氢/分析脂质过氧化作用/药物作用发光测定法磷脂类/分析大鼠 Wistar 红花油/投药和剂量硫巴比妥酸反应物/分析维生素E/投药和剂量维生素E/分析动物男(雄)性大鼠

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Hepatotoxicity of tacrine: Occurrence of membrane fluidity alterations without involvement of lipid peroxidation

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期294卷 160-167页

作者： Galisteo, M Rissel, M Sergent, O Chevanne, M Cillard, J Guillouzo, A Lagadic-Gossmann, D Univ Rennes 1 Fac Sci Pharmaceut & Biol INSERM U456 F-35043 Rennes France

Tacrine (THA), used in the treatment of Alzheimer's disease, is known to induce hepatotoxicity, the mechanisms of which remain to be fully established. We have previously shown that THA reduced intracellular glutathione concentration in rat hepatocytes in primary culture, thus pointing to a possible role for oxidative stress in THA toxicity. To test this, the effects of antioxidant molecules, namely, the flavonoids silibinin, silibinin dihydrogensuccinate, and silymarin, were evaluated on the toxicity of THA in cultured rat hepatocytes. This toxicity was investigated after a 24-h treatment over a concentration range from 0 to 1 mM, in the presence or absence of antioxidant (1 and 10 mu M). We found that simultaneous treatment of hepatocytes with any of the antioxidants and THA remained ineffective on the lactate dehydrogenase release induced by THA. Then, the production of lipid-derived radicals (to estimate lipid peroxidation) was measured in THA (0.05-0.50 mM)-treated cells using a spin-trapping technique coupled to electron paramagnetic resonance (EPR) spectroscopy. No increase of the EPR signal was observed over the period of 30 min to 24 h. In contrast, treatment of cells with the spin label 12-doxyl stearic acid followed by EPR spectroscopy showed that THA (0.05 and 0.25 mM) rapidly increased hepatocyte membrane fluidity. Extracellular application of GM1 ganglioside (60 mu M) both reversed this increase in fluidity and partially reduced lactate dehydrogenase release on THA exposure. In conclusion, this work indicates that early alterations of membrane fluidity, not resulting from lipid peroxidation, are likely to play an important role in the development of THA toxicity.

关键词：细胞培养的胆碱酯酶抑制剂/毒性电子自旋共振谱学 G(M1)神经节苷脂/药理学氢离子浓度 L-乳酸脱氢酶/分泌脂质过氧化作用/药物作用肝/药物作用膜流动性/药物作用大鼠 Sprague-Dawley 水飞蓟素/药理学他克林/毒性动物男(雄)性大鼠

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PROTECTION FROM COLD INJURY BY DEFEROXAMINE, AN IRON CHELATOR

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ANGIOLOGY 1992年第9期43卷 781-790页

作者： MAITY, S LU, D RUSSEL, JC LYENGAR, J DAS, DK UNIV CONNECTICUT SCH MEDDEPT SURGSURG RES CTRFARMINGTONCT 06030

The presence of hydroxl radical (OH.) has been implicated in the pathogenesis of cold injury. Since iron is known to catalyze the OH. formation responsible for cellular injury, this study was designed to examine whether an iron chelator such as deferoxamine can salvage a tissue from cold injury. Cold injury was induced in the hind limbs of rabbits. The experimental group received 0.6 mM of deferoxamine through the femoral vein prior to cooling of the limbs. Deferoxamine reduced the tissue injury, as evidenced by the decreased release of lactate dehydrogenase, a nonspecific marker for cellular injury. In addition, this drug inhibited OH. formation and lipid peroxidation when examined by monitoring the formation of conjugated dienes and malonaldehyde, presumptive markers for lipid peroxidation. Rewarming of the cooled limbs was also associated with the loss of membrane phospholipids, with the corresponding accumulation of lysopho-sphoglycerides and free fatty acids, especially linoleic and arachidonic acids. Deferoxamine prevented the loss of phospholipids and inhibited the accumulation of amphipathic lipid products. These results indicates that deferoxamine salvaged the tissue from cold injury, possibly by preventing the formation of OH. presumably by chelating iron, thus protecting the phospholipids from free radical attack.

关键词：去铁胺/治疗应用脂肪酸类非酯化/代谢自由基羟化物类羟自由基铁/生理学 L-乳酸脱氢酶/代谢脂质过氧化作用/药物作用膜脂质类/代谢肌/损伤肌/代谢磷脂类/代谢动物兔

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Posttreatment with ETYA protects against phosgene-induced lung injury by amplifying the glutathione to lipid peroxidation ratio

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INHALATION TOXICOLOGY 2000年第4期12卷 347-356页

作者： Sciuto, AM USA Med Res Inst Chem Def Div Pharmacol Neurotoxicol Branch Aberdeen Proving Ground MD 21010 USA

Exposure to phosgene has been shown to cause revere and life-threatening pulmonary edema. There is evidence that successful treatment of phosgene-induced acute lung injury may be related to increased antioxidant activity. Acetylenic acids such as 5,8, 11,14-eicosatetraynoic acid (ETYA) have been shown to be effective in preventing pulmonary edema formation (PEF). in phosgene-exposed guinea pigs, we examined the effects of ETYA on PEF. Lipid peroxidation (thiobarbituric acid-reactive substance, TBARS) and total glutathione (GSH) were measured in lung tissue from isolated, buffer-perfused guinea pig lungs at 180 min after start of exposure. Guinea pigs were challenged with 175 mg/m(3) (44 ppm) phosgene for 70 min (1750 mg . min/m(3)). Five minutes after removal from the exposure chamber, guinea pigs were treated, ip, with 200 mu l of 100 mu M ETYA in ethanol (ETOH). Two hundred microliters of 50 mu M ETYA in ETOH was added to the 200 mi per fusate every 40 min beginning at 60 min after start of exposure (t = 0). There were four groups in this study: air-exposed, phosgene-exposed, phosgene + ETYA-posttreated, and air + ETYA-posttreated. Posttreatment with ETYA prevented GSH depletion, 2.7 +/- 0.5 mu mol/mg protein versus 1 +/- 0.2 mu mol/mg protein, for the untreated phosgene-exposed lungs (p less than or equal to .05). ETYA posttreatment also significantly decreased PEF (p less than or equal to.025), as measured by lung wet weight/dry weight ratio, 16.1 +/- 2.5 versus 8.5 +/- 1 for phosgene-exposed + ETYA-posttreated guinea pigs. Postexposure treatment with ETYA significantly increased the GSH to TBARS protection ratio, 12 +/- 2, compared with the phosgene-exposed group, 3.7 +/- 0.5 (p less than or equal to.05). in conclusion, ETYA posttreatment decreased PEF by increasing the GSH/TBARS protection ratio by functioning in an antioxidant-like capacity.

关键词： 5 8 11 14-花生四烯酸/投药和剂量 5 8 11 14-花生四烯酸/治疗应用投药吸入谷胱甘肽/代谢注射腹腔内脂质过氧化作用/药物作用肺/药物作用肺/代谢肺/病理学器官测量/药物作用光气/投药和剂量光气/毒性肺水肿/化学诱导肺水肿/预防和控制动物豚鼠男(雄)性

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