云南甘草总皂甙清除氧自由基和抗脂质过氧化作用

云南甘草总皂甙(SGY)对Fenton反应生成的·OH具有较强的直接清除作用,其IC_(50)为29mg·L~(-1).且作用明显强于·OH特异性清除剂甘露醇(其IC_(50)为2.27×10~(-2)mol·L~(-1).即4315mg·L~(-1))。SGY对黄嘌呤-黄嘌呤氧化酶系统产生的O_2~+也有较强的清除作用·其IC_(50)为89mg·L~(-1)SGY对自由基发生系统(FRGS)诱导离体大鼠心肌匀浆组织产生的脂质过氧化(LPO)作用有明显的抑制效应.对FRGS诱导离体大鼠心肌线粒体膜LPO也有一定的抑制作用。结果提示SGY的抗脂质过氧化作用与其清除氧自由基作用有关。     

几种香茶菜属二萜类化合物的抗氧化作用

目的　了解香茶菜属二萜类化合物冬凌草乙素(Pon)、香茶菜醛 (Ame)、毛叶香茶菜醇 (Iso)是否具有抗氧化作用。方法　用分光光度法测定Fenton反应体系中细胞色素C(Ⅱ )的含量 ,了解清除·OH的能力 ;用紫外分光光度法测定N-2 的含量 ,了解清除O-·2 的能力 ,用DTNB法测定GSH的含量。结果　Orid、Pon、Ame、Iso ,5 0、10 0、2 0 0 μmol·L-1可清除H2 O2 Fe2 + 反应体系中产生的·OH ,且呈剂量依赖关系。Orid、Pon、Ame、Iso ,4 0 0、80 0 μmol·L-1可清除黄嘌呤 -黄嘌呤氧化酶系统产生的NO-2 。Orid、Pon、Ame、Iso ,1、2 μmol·L-1可明显的减少LPS刺激巨噬细胞产生的NO-2 。Orid、Pon、Ame、Iso ,2、4 μmol·L-1可明显抑制CCl4造成的GSH含量降低 ,具有剂量依赖性。结论　Orid、Pon、Ame、Iso能有效地清除羟自由基和一氧化氮 ,抑制脂质过氧化而产生抗氧化作用     

Protective Actions of Blumea Flavanones on Primary Cultured Hepatocytes and Liver Subcellular Organelle against Lipid Peroxidation

目的：研究艾纳香二氢黄酮对脂质过氧化致损伤的恒河猴原代培养肝细胞及肝亚细胞的保护作用。方法：艾纳香二氢黄酮与原代培养肝细胞共育后，以ＣＣｌ４或ＦｅＳＯ４半胱氨酸致细胞损伤，以脂质过氧化产物丙二醛产生量及转氨酶的漏出量作为损伤程度指标。亚细胞结构与艾纳香二氢黄酮共育后，以ＦｅＳＯ４半胱氨酸致脂质过氧化，以丙二醛产生量衡量过氧化损伤程度。结果：１０及１００μｍｏｌ·Ｌ１的艾纳香二氢黄酮可降低被损伤的肝细胞中的丙二醛产生，降低转氨酶漏出，抑制肝亚细胞结构中丙二醛生成。结论：艾纳香二氢黄酮具有抑制脂质过氧化作用及肝细胞、亚细胞结构保护作用     

海绵polymistia spongia提取物aldisin的抗脂质过氧化及清除自由基作用研究

目的研究海绵ｐｏｌｙｍｉｓｔｉａｓｐｏｎｇｉａ提取物ａｌｄｉｓｉｎ的抗脂质过氧化及清除自由基作用。方法采用ＭＤＡ－ＴＢＡ比色法测定组织匀浆中过氧化脂质（ＬＰＯ）含量；采用邻苯三酚自氧化法测定ａｌｄｉｓｉｎ对Ｏ·２自由基的清除作用；采用分光光度法测定ａｌｄｉｓｉｎ对Ｃｕ２＋－ＶｉｔＣ体系产生的·ＯＨ自由基的清除作用；采用ＥＳＲ法测定ａｌｄｉｓｉｎ对ＤＰＰＨ自由基的清除作用。结果ａｌｄｉｓｉｎ具有显著的抗脂质过氧化作用，并能有效地清除Ｏ·２、·ＯＨ和ＤＰＰＨ自由基，在０．４２６μｍｏｌ·Ｌ－１～１８．５ｍｍｏｌ·Ｌ－１浓度范围内有明显的量效关系。结论ａｌｄｉｓｉｎ是自由基清除剂。     

艾纳香二氢黄酮对大鼠实验性肝损伤的保护作用

艾纳香二氢黄酮对大鼠实验性肝损伤的保护作用许实波赵金华（中山大学药学系药理学教研室，广州５１０２７５）中国图书分类号Ｒ２８４．１；Ｒ９７５．５艾纳香二氢黄酮（ｂｌｕｍｅａｆｌａｖａｎｏｎｅｓ，ＢＦｓ）包括５种化合物，本文分别命名为ＢＦ－Ⅰ、ＢＦ－Ⅱ、...     

穿心草口山酮抗氧化作用初探

目的以大鼠组织匀浆及ＲＢＣ为材料研究３种穿心草口山酮（ｘａｎｔｈｏｎｅ，Ｘａｎ）：１，８－ｄｉｈｙｄｒｏｘｙ３，５－ｄｉｍｅｔｈｏｘｙｘ－ａｎｔｈｏｎｅ（Ｘａｎ－Ⅰ）；１－ｈｙｄｒｏｘｙ，５－ｄｉｍｅｔｈｏｘｙｘａｎｔｈｏｎｅ（Ｘａｎ－Ⅱ）；１－ｈｙｄｒｏｘｙ，３，７，８－ｔｒｉｔｈｏｘｙｘａｎｔｈｏｎｅ（Ｘａｎ－Ⅲ）抗脂质过氧化作用。方法以ＭＤＡ为指标，观察Ｘａｎ对组织匀浆体外脂质过氧化及ＲＢＣ自氧化溶血体系脂质过氧化产物丙二醛（ＭＤＡ）生成量的影响；并观察Ｘａｎ对邻苯三酚自氧化产生的Ｏ·２及Ｃｕ２＋－ＶｉｔＣ自由基产生系统产生的·ＯＨ的清除作用。结果①０．０５μｍｏｌ·Ｌ－１的３种Ｘａｎ均可抑制正常大鼠脑、肝、心匀浆体外过氧化脂质生成，并能对抗半胱氨酸和硫酸亚铁所致过氧化脂质生成增加。②３种Ｘａｎ均能抑制ＲＢＣ自氧化，显著减少ＲＢＣ自氧化过程中ＭＤＡ的含量。③３种Ｘａｎ均能清除超氧阴离子自由基（Ｏ·２）和羟自由基（·ＯＨ），清除·ＯＨ的作用更强。④３种Ｘａｎ清除氧自由基的活性强弱顺序为Ｘａｎ－Ⅰ＞Ｘａｎ－Ⅲ＞Ｘａｎ－Ⅱ。结论穿心草口山酮具有一定的抗氧化作用，能直接清除活性氧自由基。     

茶多酚清除氧自由基及抑制脑脂质过氧化反应的体外试验

目的研究茶多酚对羟自由基（·ＯＨ）、超氧阴离子自由基（Ｏ·２）的清除作用及其对脂质过氧化的抑制作用。方法茶多酚与自由基发生体系或大鼠脑线粒体共浴后，比色法测定·ＯＨ、Ｏ·２及丙二醛生成量。结果茶多酚对Ｆｅｎｔｏｎ反应生成的·ＯＨ及黄嘌呤－黄嘌呤氧化酶系统产生的Ｏ·２具有较强的清除作用，ＩＣ５０分别为９１９．６ｍｇ·Ｌ－１和８３６ｍｇ·Ｌ－１。茶多酚对·ＯＨ诱导的离体大鼠脑线粒体产生的脂质过氧化有明显的抑制作用。结论茶多酚的抗脂质过氧化作用与其清除氧自由基作用有关     

排毒养颜胶囊对非酶体系产生的·OH及O·2的清除作用

目的:通过对活性氧自由基的清除作用研究排毒养颜胶囊排毒养颜的部分作用机理.方法:用化学发光法测定该中药方剂水浸提液对非酶体系产生的超氧阴离子自由基()和羟自由基(·OH)的清除作用.结果:该浸提液清除的SC50为2.7×10-5g·ml-1,相当于10 ng·ml-1 SOD的活性;清除·OH的SC50为6.5×10-5g·ml-1,相当于1×10-5 mol·L-1硫脲的活性.当浸提液浓度较高时,它对和.OH的清除率均可达90%以上.结论:这种较强的抗自由基活性可能是该中药方剂排毒养颜的部分作用机理.     

排毒养颜胶囊对非酶体系产生的·OH及的清除作用

目的 :通过对活性氧自由基的清除作用研究排毒养颜胶囊排毒养颜的部分作用机理。方法 :用化学发光法测定该中药方剂水浸提液对非酶体系产生的超氧阴离子自由基 (O ·2 )和羟自由基 (·OH)的清除作用。结果 :该浸提液清除O ·2 的SC5 0 为 2 7× 1 0 5 g·ml 1 ,相当于 1 0ng·ml 1 SOD的活性 ;清除·OH的SC5 0 为 6 5× 1 0 5 g·ml 1 ,相当于 1× 1 0 5 mol·L 1 硫脲的活性。当浸提液浓度较高时 ,它对O ·2 和·OH的清除率均可达 90 %以上。结论 :这种较强的抗自由基活性可能是该中药方剂排毒养颜的部分作用机理     

内南五味子木脂素戈米辛J对肝线粒体膜脂质过氧化和超氧阴离子自由基的作用

目的　研究来自内南五味子的戈米辛J对脂质过氧化的影响和清除超氧阴离子自由基 (O·2 )的能力。方法　采用离体大鼠肝线粒体膜的脂质过氧化模型和黄嘌呤氧化酶 鲁米诺化学发光法。结果　戈米辛J象VitE一样能剂量依赖性抑制Fe2 + VitC和ADP/NADPH所致的脂质过氧化 ;戈米辛J的IC50 分别为 5 75 ( 95 %可信限 :5 42～ 6 11)和0 95 ( 0 14～ 6 5 4) μmol·L-1。VitE的IC50 分别为 74 8( 30 2～ 185 3)和 6 5 1( 0 13～ 319) μmol·L-1。戈米辛J抑制Fe2 + VitC和ADP/NADPH所致的脂质过氧化的作用比VitE的作用分别强 13倍和 6 8倍。戈米辛J也剂量依赖地抑制黄嘌呤 黄嘌呤氧化酶 鲁米诺化学发光 ,其抑制发光强度 5 0 %的浓度 (IC50 )为 2 18 2 2 μmol·L-1。结论　戈米辛J具有抑制OH·诱导的脂质过氧化和清除O·2 的作用     

甘草类黄酮对脂质过氧化和活性氧自由基的作用

本文用比色法测定过氧化脂质研究甘草类黄酮(FG)的抗脂质过氧化作用,并用化学发光法和自旋捕集技术检测该药对O₂^-和OH^·的清除作用。体外实验表明:FG 2.8～25μg/ml可明显抑制小鼠肝匀浆在振荡温育条件下引起的丙二醛升高;FG 0.265～26.5μg/ml或2.58～258 μg/ml分别对碱性二甲基亚砜或黄嘌呤/黄嘌呤氧化酶体系生成的O₂^-有显著清除作用;以上作用呈浓度依赖性变化。FG 144 μg/ml或258 μg/ml分别对PMA刺激多形核白细胞释放的O₂^-及OH^·或Fenton's反应生成的OH^·有明显清除作用。实验证明FG有抗氧化作用。     

山楂叶总黄酮对血管内皮细胞氧化损伤的保护作用

目的：研究溶血磷脂酰胆碱（LPC）和氧自由基（OFR）对血管内皮细胞（VEC）的损伤，及山楂叶总黄酮对损伤后VEC的保护作用。方法：以体外培养的小牛主动脉内皮细胞为材料，测定LPC或黄嘌呤和黄嘌呤氧化酶（X XO）与VEC的作用，以及加入不同浓度的山楂叶总黄酮后，对细胞乳酸脱氢酶（LDH）的泄漏量，细胞丙二醛（MDA）和一氧化氮（NO）的含量及对细胞增殖的影响。结果：当VEC与LPC（5ug/ml)或黄嘌呤和黄嘌呤氧化酶（X XO）（10umol/L 200umol/L)共孵育24h时，表现为细胞LDH泄漏量增多，细胞内MDA含量升高，NO含量减少，细胞生长减缓，存活率下降；当加入不同浓度的山楂叶总黄酮后则可明显抑制细胞LDH的泄漏量，降低MDA含量，提高NO的含量，细胞生长正常，存活率提高，结论：山楂叶总黄酮能通过抗氧化途径对LPC与X XO所致VEC的氧化损伤起保护作用。     

Cellular mechanism of U78517F in the protection of porcine coronary artery endothelial cells from oxygen radical-induced damage.

1. The aim of this study was to clarify the role of lipid peroxidation in cellular injury as assessed by lactate dehydrogenase (LDH) release from cultured coronary artery endothelial cells of the pig. Cells exposed to H2O2 at concentrations of 0.1 to 20 mM or to a xanthine and xanthine oxidase (X/XO) reaction mixture released LDH into the medium. Significant release from X/XO-treated cells took place with a delay of 2 h. 2. Superoxide dismutase (SOD), catalase or dimethylthiourea attenuated the release of LDH from X/XO-treated cells. Similarly the putative inhibitor of lipid peroxidation, U78517F attenuated the release of LDH by X/XO with an IC50 of 0.08 microM. 3. H2O2 was continuously produced by the addition of X/XO to the medium alone. However, in the presence of endothelial cells, H2O2 was eliminated at 1 h. U78517F had no effect on either process. 4. The oxygen radical-induced release of LDH was associated with malondialdehyde (MDA) formation. U78517F inhibited the formation of MDA with an IC50 of 0.27 microM. 5. Reduction of the Ca2+ concentration in the incubation medium from 1.6 mM to 0.016 mM markedly attenuated the release of LDH from endothelial cells. Nifedipine (1 microM) did not attenuate the LDH release from the cells. 6. It is likely that porcine coronary artery endothelial cells can be thus injured by oxygen radicals presumably through hydroxyl radicals formed and consequent lipid peroxidation, and that the extracellular Ca2+ concentration plays an important role in the genesis of such endothelial cell damage.     

The influence of lipid peroxidation products (malondialdehyde, 4-hydroxynonenal) on xanthine oxidoreductase prepared from rat liver.

Depending on metabolic conditions, xanthine oxidoreductase acts as either a dehydrogenase (XDH) or an oxidase (XOD). The metabolism of hypoxanthine and xanthine by the oxidase is associated with the production of reactive oxygen radicals. Reaction of reactive oxygen radicals with polyunsaturated fatty acids (lipid peroxidation) leads to the formation of malondialdehyde (MDA) and 4-hydroxynonenal (HNE), known to modify proteins by reaction with NH2- and SH-groups. Therefore, these aldehydes could influence both the activity of xanthine oxidoreductase and the XOD/XDH ratio. We found that incubation of xanthine oxidoreductase with MDA leads to an initial increase in XDH activity and to a continuous decrease in XOD activity, whereby the total activity decreases. This was in contrast to the effects of HNE which did not alter the XDH activity; XOD was however activated. This demonstrates that the lipid peroxidation products MDA and HNE are able to modify xanthine oxidoreductase similarly to a feed-back mechanism.     

Antioxidative activity of natural isorhapontigenin.

Isorhapontigenin (ISOR), isolated from Belamcanda chinensis, is a derivative of stilbene. Its chemical structure is very similar to that of resveratrol, with a potent antioxidative effect. In the present study, we investigated the antioxidative activity of ISOR in vitro. Oxidative damage of rat liver microsomes, brain mitochondria and synaptosomes was induced by Fe2+-Cys, VitC-ADP-Fe2+ and H2O2, respectively. The formation of malondialdehyde (MDA), decrease of reduced glutathione (GSH) and increase of ultra-weak chemiluminescence during the lipid peroxidation process were determined. In addition, the characteristic ultra-weak chemiluminescence of oxidative DNA damage induced by CuSO4-Phen-VitC-H2O2 system was studied. The results showed that ISOR significantly inhibited MDA formation in liver microsomes, brain mitochondria and synaptosomes induced by Fe2+-Cys. Also, ISOR markedly prevented the decrease of GSH in mitochondria and synaptosomes induced by H2O2 and the increase of ultra-weak chemiluminescence during lipid peroxidation induced by VitC-ADP-Fe2+ as well as oxidative DNA damage induced by CuSO4-Phen-VitC-H2O2. The effects of ISOR at 10(-5) and 10(-6) mol/L on the MDA formation and decrease of GSH were similar to that of the classical antioxidant vitamin E (10(-4) mol/L). It may be concluded that ISOR possessed potent antioxidative activity and was much more potent than vitamin E.     

d-儿茶素-3-O-β-D-葡萄糖苷的抗氧化作用(英文)

目的　研究粘萎陵菜含有的一种化合物 ,d 儿茶素 3 O β D 葡萄糖苷 (CGS)的保肝作用机制。方法　测定CGS在体外对NADPH 维生素C和Fe2 + 半胱氨酸系统诱发的微粒体脂质过氧化反应(丙二醛形成 )的影响 ,对黄嘌呤 黄嘌呤氧化酶系统超氧阴离子自由基产生 (还原型细胞色素C形成 )的影响 ;在体内对CCl4和乙醇诱发的小鼠肝丙二醛形成的影响。结果　体外CGS 1 0 0 μmol·L-1 能明显抑制NADPH 维生素C和Fe2 + 半胱氨酸系统诱发的大鼠脑、肝、肾微粒体丙二醛形成及黄嘌呤 黄嘌呤氧化酶系统超氧阴离子自由基的产生。在体内能抑制CCl4和乙醇诱发的小鼠肝脂质丙二醛形成。结论　CGS具有抗氧化作用     

Does luminol chemiluminescence detect free radical scavengers?

Thiol compounds have been reported to abolish hypoxanthine/xanthine oxidase induced luminol chemiluminescence and this effect has been attributed to scavenging of superoxide (O2-)/(H2O2) produced from hypoxanthine/xanthine oxidase. Yet other workers have reported that thiol compounds have shown little, if any, reactivity towards O2-/H2O2. The aim of this study was to examine the discrepancy between these two sets of findings further. Captopril (a thiol angiotensin-converting enzyme (ACE) inhibitor) and MPG (a simple thiol) were observed to abolish hypoxanthine/xanthine oxidase induced chemiluminescence. The reactivity of captopril and MPG towards O2-/H2O2 was then determined by measurement of thiol oxidation in captopril and MPG after their incubation with hypoxanthine/xanthine oxidase. Incubation (at 10 min, 37 degrees C) with 4 mM hypoxanthine/0.03 u ml-1 xanthine oxidase resulted in 7% and 20% thiol oxidation in captopril and MPG (at 1 mM) respectively. Captopril and MPG, therefore, appeared to be ineffective scavengers of oxidants produced by hypoxanthine/xanthine oxidase. Captopril and MPG also did not affect urate production or oxygen consumption by xanthine oxidase which indicated that captopril and MPG quench luminol chemiluminescence by a mechanism that excludes the inhibition of xanthine oxidase. Hypoxanthine/xanthine oxidase induced luminol chemiluminescence may, therefore, be an unsuitable method for measuring free radical scavenging activity by drugs.     

Stimulation of the active transport of serotonin into human platelets by hydrogen peroxide

The effect of H2O2 on the active transport of serotonin (5-HT) by human platelets was investigated. Platelets were exposed to either a single dose of H2O2 or to H2O2 generated by the glucose/glucose oxidase or xanthine/xanthine oxidase enzyme systems. H2O2 (12.5 to 100 microM) produced a rapid, concentration-dependent and time-dependent increase in 5-HT transport which was maximal after a 2-min incubation and decreased with continued incubation. Catalase (1000 units) completely prevented H2O2-induced stimulation, and fluoxetine (1 microM) totally blocked 5-HT uptake into stimulated platelets. The glucose/glucose oxidase (3.12 to 100 milliunits) and the xanthine/xanthine oxidase system, superoxide dismutase (250 units) failed to alter the stimulation, whereas catalase (1000 units) effectively prevented the response. The kinetics of 5-HT transport indicated that H2O2 treatment did not alter the Km of 5-HT transport (Km control = 1.0 +/- 0.2 x 10(-6) M vs Km H2O2 = 1.1 +/- 0.1 x 10(-6) M) but markedly increased the maximal rate of 5-HT transport (Vmax control = 131.4 +/- 4.6 pmol/10(8) platelets/4 min vs Vmax H2O2 = 206.7 +/- 9.1 pmol/10(8) platelets/4 min). These data demonstrated that exposure of human platelets to H2O2 resulted in a stimulation of the active transport of 5-HT and suggested that H2O2 may function to regulate this process.     

Picroliv, picroside-I and kutkoside from Picrorhiza kurrooa are scavengers of superoxide anions.

Picroliv, the active principle of Picrorhiza kurrooa, and its main components which are a mixture of the iridoid glycosides, picroside-I and kutkoside, were studied in vitro as potential scavengers of oxygen free radicals. The superoxide (O2-) anions generated in a xanthine-xanthine oxidase system, as measured in terms of uric acid formed and the reduction of nitroblue tetrazolium were shown to be suppressed by picroliv, picroside-I and kutkoside. Picroliv as well as both glycosides inhibited the non-enzymic generation of O2- anions in a phenazine methosulphate NADH system. Malonaldehyde (MDA) generation in rat liver microsomes as stimulated by both the ascorbate-Fe2+ and NADPH-ADP-Fe2+ systems was shown to be inhibited by the Picroliv glycosides. Known antioxidants tocopherol (vitamin E) and butylated hydroxyanisole (BHA) were also compared with regard to their antioxidant actions in the above system. It was found that BHA afforded protection against ascorbate-Fe(2+)-induced MDA formation in microsomes but did not interfere with enzymic or non-enzymic O2- anion generation; and tocopherol inhibited lipid peroxidation in microsomes by both prooxidant systems and the generation of O2- anions in the non-enzymic system but did not interfere with xanthine oxidase activity. The present study shows that picroliv, picroside-I and kutkoside possess the properties of antioxidants which appear to be mediated through activity like that of superoxide dismutase, metal ion chelators and xanthine oxidase inhibitors.