绞股蓝多糖体外抗氧化活性研究

研究绞股蓝多糖的单糖组成及抗氧化活性.采用气相色谱(GC)分析绞股蓝多糖的单糖组成,通过体外抗氧化评价体系研究绞股蓝粗多糖(GPMPP)和精制多糖(GPMP)的总还原力、清除DPPH自由基、羟自由基的活性以及抗脂质过氧化作用.结果显示,绞股蓝多糖由鼠李糖、阿拉伯糖、木糖、甘露糖、葡萄糖和半乳糖组成,物质的量比为1.39∶3.76∶1.00∶1.64∶4.98∶5.88.绞股蓝多糖具有较好的还原能力,对DPPH自由基和·OH具有较强的清除能力,并且对小鼠肝匀浆自发性脂质过氧化和Fe2+-H2O2诱导的小鼠肝匀浆脂质过氧化具有较好的抑制作用.以上结果表明,绞股蓝多糖具有明显的抗氧化活性.     

灵芝孢子副产物体外抗氧化活性的研究

利用有机溶剂萃取法获得灵芝孢子副产物五个不同极性部位,以总抗氧化能力(T-AOC)及羟自由基(·OH)和2,2-二(4-叔辛基苯基)-1-苦肼基自由基(DPPH·)的清除能力为评价指标筛选最优抗氧化活性部位,并对其进行抗脂质过氧化研究,结果显示:不同极性部位均能清除上述自由基,其中乙酸乙酯相活性最强。进一步研究发现,乙酸乙酯相能够显著抑制β-胡萝卜素/亚油酸体系,同时对小鼠肝脏自氧化及H2O2诱导的肝脂质过氧化和红细胞过氧化溶血均有较好保护作用。实验表明:灵芝孢子副产物不同极性部位提取物均具一定程度的抗氧化活性,其中乙酸乙酯相活性最强。     

灵芝孢子副产物体外抗氧化活性的研究北大核心CSCD

利用有机溶剂萃取法获得灵芝孢子副产物五个不同极性部位,以总抗氧化能力(T-AOC)及羟自由基(·OH)和2,2-二(4-叔辛基苯基)-1-苦肼基自由基(DPPH·)的清除能力为评价指标筛选最优抗氧化活性部位,并对其进行抗脂质过氧化研究,结果显示:不同极性部位均能清除上述自由基,其中乙酸乙酯相活性最强。进一步研究发现,乙酸乙酯相能够显著抑制β-胡萝卜素/亚油酸体系,同时对小鼠肝脏自氧化及H2O2诱导的肝脂质过氧化和红细胞过氧化溶血均有较好保护作用。实验表明:灵芝孢子副产物不同极性部位提取物均具一定程度的抗氧化活性,其中乙酸乙酯相活性最强。     

3'-大豆苷元磺酸钠的体外抗氧化研究

为研究3'-大豆苷元磺酸钠(DSS)的体外抗氧化活性,测定了DSS对超氧自由基(O2·)、羟基自由基(·OH)和1,1-二苯基-2.苦苯肼自由基(DPPH·)的清除能力,及其对Fe2 诱导的脂质过氧化反应和β-胡萝卜素/亚油酸自氧化体系的抑制作用.结果表明,DSS对DPPH·有一定的清除能力,对超氧自由基的清除能力较强,能很好地清除·OH自由基,对脂质过氧化有一定的抑制作用,对β-胡萝卜素/亚油酸自氧化体系有明显的抑制作用.说明DSS的药理作用可能与其较强的抗氧化能力有关.     

甘青铁线莲花水提取物的抗氧化活性研究

本文采用邻二氮菲-Fe2 氧化法,邻苯三酚自氧化法以及卵黄脂蛋白不饱和脂肪酸(PUFA)过氧化体系,对甘青铁线莲花水提取物清除超氧阴离子自由基(O-·2 )和羟自由基(·OH )以及抑制卵黄脂蛋白脂质过氧化(LPO)作用的效果进行了测定.结果表明:甘青铁线莲花水提取物有清除O-2、OH的能力,同时能抑制卵黄脂蛋白脂质过氧化(LPO)作用,在相同干物质浓度下(黄酮含量为2.20 μg),抑制卵黄脂蛋白脂质过氧化(LPO)作用最强、O-2次之、OH最弱,这说明甘青铁线莲花水提取物有抗氧化作用,且水提物抗氧化活性在一定浓度范围内与其黄酮类化合物含量呈正相关.     

滑子菇多糖的体外生物活性初步研究

为了研究滑子菇水提粗多糖(PNP)的体外生物活性,对滑子菇多糖的总还原力、清除1,1-二苯基-2-苦苯肼自由基(DPPH·)和由Fe2+诱发的脂质过氧化反应的抑制作用进行研究,采用MTT比色法和胎盘蓝细胞计数检测对滑子菇水提粗多糖的体外抑制K562细胞生长作用进行了研究,采用流失细胞术对滑子菇多糖作用人白血病K562细胞后的细胞周期进行了研究。结果表明:滑子菇水提粗多糖PNP具有一定的还原能力;在高质量浓度(800μg/mL)时具有接近于Vc清除DPPH·的能力,达41.28%;PNP对Fe2+诱发的脂质过氧化反应具有一定的抑制作用,并且随着浓度的增加抑制作用逐渐增强,但总的增长趋势不大;MTT实验表明PNP对K562细胞的体外增长有抑制作用,在质量浓度为800μg/mL和作用时间为48 h时,可达到最高的抑制率35.03%。流式细胞术对细胞周期的检测表明滑子菇多糖能够阻滞人白血病K562细胞于G1期。     

冬葵果多糖的抗氧化作用研究

研究冬葵果多糖(Fructus Malvae polysaccharides,FMP)对氧自由基的清除作用及对脂质过氧化的抑制作用。采用分光光度法测定FMP清除Fenton体系产生的羟自由基(.OH)、邻苯三酚自氧化体系产生的超氧阴离子自由基(O2-.)的能力及评价对Fe(Ⅱ)-H2O2体系(.OH)诱导的脂质过氧化终产物丙二醛(MDA)的抑制作用。结果显示,在化学模拟体系中,冬葵果多糖对.OH具有很强的清除作用,与VC比较达到显著水平(P<0.01),对O2-.的清除能力与VC相当。在体外,多糖浓度达到1.72 mg/mL可明显降低MDA的含量,与空白液比较达到显著水平(P<0.01)。以上结果表明,FMP具有明显的抗氧化活性。     

南瓜醇提物的体外抗氧化活性(英文)

采用化学体系模拟法体外测定南瓜醇提物((pumpkin ethanol extract,PEE)对1,1-二苯基-2-苦苯肼自由基(DPPH·)、超氧阴离子自由基(O2)和羟自由基(·OH)的清除能力,总还原力,对β-胡萝卜素/亚油酸自氧化体系的总抗氧化能力以及脂质过氧化的抑制能力.结果显示PEE对DPPH·、02-和·OH均有较强的清除能力,IC50值分别为18.8 mg/mL、29.0 ms/mL和44.9μg/mL,有显著的还原力和总抗氧化力,对脂质过氧化有一定的抑制作用.PEE的体外抗氧化活性均有良好的量效关系.上述结果为南瓜作为抗氧化的保健食品或功能食品开发利用提供了依据.     

桂丁、草蔻挥发油抗氧化性研究

采用脂质过氧化方法和DPPH方法分别检测了2种植物挥发油抗脂质过氧化活性和清除自由基活性.且通过和阳性对照Vitamin E和Vitamin C的比较发现2种植物挥发油均有不同程度的抗脂质过氧化活性和清除自由基的活性.草蔻的抗脂质过氧化活性在低浓度下抑制率很高,在浓度为0.097～1.2 mg/mL之间其抗氧化能力强于桂丁.用IC50和EC50来评价抗脂质过氧化能力和清除自由基活性,则草蔻挥发油的抗脂质过氧化活性最强,且强于阳性对照Vitamin C,即草蔻的IC50为0.099 mg/mL.对于草蔻和桂丁的清除自由基的能力是相似的,EC50分别为4.50和4.46 mg/mL.     

不同提取方法对桔梗多糖体外抗氧化性的影响

本实验考查热水浸提法、超声波提取法、微波提取法和复合酶提取法在提取桔梗多糖时对其活性所产生的影响。在模拟体外抗氧化条件下,从总还原能力、清除超氧阴离子能力、清除羟自由基能力、清除DPPH·自由基能力和体外抗肝组织自发性脂质过氧化能力等五个方面,对不同方法提取的桔梗多糖的抗氧化活性进行了分析和评估。结果表明:微波法提取的桔梗多糖体外抗氧化效果最好且差异显著(P0.01)。此方法提取的桔梗多糖对羟自由基、DPPH·自由基的清除和对脂质过氧化作用的抑制均具有较强效果,其最大多糖浓度的清除率或抑制率均接近或超过50%,但对超氧阴离子自由基的清除能力相对较弱,最大清除率仅有25%。     

Carvedilol inhibition of lipid peroxidation. A new antioxidative mechanism

To define the molecular mechanism(s) of carvedilol inhibition of lipid peroxidation we have utilized model systems that allow us to study the different reactions involved in this complex process.

Carvedilol inhibits the peroxidation of sonicated phosphatidylcholine liposomes triggered by FeCl₂ addition whereas atenolol, pindolol and labetalol are ineffective. The inhibition proved not to be ascribable (a) to an effect on Fe²⁺ autoxidation and thus on the generation of oxygen derived radical initiators; (b) to the scavenging of the inorganic initiators O^·-₂ and ^·OH; (c) to an effect on the reductive cleavage of organic hydroperoxides by FeCl₂; (d) to the scavenging of organic initiators. The observations that (a) carvedilol effectiveness is inversely proportional to the concentration of FeCl₂ and lipid hydroperoxides in the assay; (b) the drug prevents the onset of lipid peroxidation stimulated by FeCl₃ addition and; (c) it can form a complex with Fe³⁺, suggest a molecular mechanism for carvedilol action. It may inhibit lipid peroxidation by binding the Fe³⁺ generated during the oxidation of Fe²⁺ by lipid hydroperoxides in the substrate. The lag time that carvedilol introduces in the peroxidative process would correspond to the time taken for carvedilol to be titrated by Fe³⁺; when the drug is consumed the Fe³⁺ accumulates to reach the critical parameter that stimulates peroxidation. According to this molecular mechanism the antioxidant potency of carvedilol can be ascribed to its ability to bind a species, Fe³⁺, that is a catalyst of the process and to its lipophilic nature that concentrates it in the membranes where Fe³⁺ is generated by a site specific mechanism.     

Novel antioxidants isolated from plants of the genera Ferula, Inula, Prangos and Rheum collected in Uzbekistan

We examined the effects of 48 compounds isolated from Ferula pallida, F. penninervis, Inula macrophylla, Prangos pabularia, P. tschimganica and Rheum maximowiczii collected in Uzbekistan on ADP/Fe²⁺-induced lipid peroxidation of egg yolk phosphatidylcholine liposomes. Of those compounds, 23 inhibited ADP/Fe²⁺-induced lipid peroxidation and nine showed especially strong inhibition of lipid peroxidation. Most compounds that inhibited peroxidation scavenged the 1,1′-diphenyl-2-picrylhydrazyl (DPPH) radical, indicating that the inhibition was due to radical scavenging. However, some compounds did not scavenge DPPH but inhibited lipid peroxidation significantly, suggesting that their inhibitory effect was not due to radical scavenging but to some other mechanism, such as prevention of Fe²⁺ function. Thus, we found various new antioxidants, some of which had a unique mechanism of action, in Ferula, Inula, Prangos and Rheum plants collected in Uzbekistan as seeds used in medicine.     

Morphology,Solid Structure and Antioxidant Activity in Vitro of Angelica sinensis Polysaccharide-Ce(IV)

Angelica Sinensis polysaccharide cerium (ASP−Ce) was prepared by Angelica Sinensis polysaccharide (ASP) and cerium ammonium nitrate (NH₄)₂Ce(NO₃)₆. and its morphology, and solid structure was investigated. The antioxidant activity of the ASP−Ce complex in vitro was evaluated. The antioxidant activity of ASP−Ce complex in vitro was evaluated by the scavenging activity of 2,2-diphenyl-1-picrylhyrazyl radical (DPPH), hydroxyl radical (⋅OH) and superoxide anion radical ( ⋅). The results showed that the ASP−Ce had the more ordered structure for inserting the Ce⁴⁺ into the polymer chain of ASP and there was little change in the conformation of the polysaccharide from Ce⁴⁺. Three free radical scavenging experiments proved that ASP−Ce had better antioxidant capacity than of ASP, especially on DPPH, and then on ⋅. The scavenging rate of ASP−Ce at 1.0 mg/mL on DPPH reached 71.6 %. Therefore, these results provide references for the further development and utilization of rare earth-polysaccharide.     

An investigation into thee mechanism of citrate---FE-dependent lipid peroxidation

Chelation by citrate was found to promote the autoxidation of Fe²⁺, measured as the disapperance of 1,10-phenanthroline-chelatable Fe²⁺. The autoxidation of citrate---²⁺ could in turn promote the peroxidation of microsomal phospholipid liposomes, as judged by malondialdehyde formation. At low citrate---Fe²⁺ ratios the autoxidation of Fe²⁺ was slow and the formation of malondialdehyde was preceded by a lag phase. The lag phase evidence of this, linear initial rates of lipid peroxidation were obtained via the combination of citrate---Fe²⁺ and citrate---Fe³⁺, optimum activity occurring at a Fe³⁺---Fe²⁺ ratio of 1:1. Evidence is also presented to suggest that the superoxide and the hydrogen peroxide that are formed during the autoxidation of citrate---Fe²⁺ can either stimulate or inhibit lipid peroxidation by affecting the yield of citrate---Fe³⁺ from citrate---Fe²⁺. No evidence was obtained for the participation of the hydroxyl radical in the initiation of lipid peroxidation by citrate---Fe²⁺.     

蝉虫草菌丝体胞内和胞外多糖抗肝细胞氧化损伤比较研究

蝉虫草（蝉花）作为我国传统的中药材,是一种药食两用的虫生真菌,因含有丰富的活性物质而具有广泛的医疗保健价值。本研究以自由基清除率为指标分析蝉虫草胞内和胞外多糖的化学抗氧化活性,再以H₂O₂诱导的人肝LO2细胞氧化损伤为模型,进而分析比较二者对肝细胞氧化应激损伤的改善作用。结果表明,在化学抗氧化能力比较上,蝉虫草菌丝体胞外多糖有效清除?OH自由基、ABTS自由基和DPPH自由基的EC₅₀值分别为1.06mg/mL、0.96mg/mL和0.63mg/mL,而胞内多糖的EC₅₀值分别为3.71mg/mL、2.83mg/mL和1.70mg/mL,表明蝉虫草胞外多糖的化学抗氧化能力更强;在改善细胞氧化应激损伤比较上,与模型组对比,二者均能随着浓度递增而显著地提高细胞存活率,但胞外多糖比胞内多糖更强,当多糖浓度为5mg/mL时,胞外多糖细胞存活率达到92.36%,胞内多糖只达到82.07%;在调节细胞抗氧化酶清除ROS的机制上,与模型组对比,胞外多糖分别上调SOD酶活力2.51倍和CAT酶活力2.91倍,极显著地降低了细胞ROS水平（P<0.01）来改善细胞的氧化应激损伤作用。相应地,胞内多糖只上调了1.85倍和2.33倍,显著性地清除了ROS（P<0.05）,表明蝉虫草菌丝体胞外多糖具有更显著的抗肝细胞氧化损伤作用。本研究结果显示蝉虫草菌丝体胞外和胞内多糖均具有良好的抗肝氧化损伤活性,且胞外多糖比胞内多糖活性更好,为蝉虫草菌丝体多糖在保肝产品中的开发和应用提供了科学依据。     

松栎柱锈菌春孢子多糖体外抗氧化活性

为了研究松栎柱锈菌（Cronartium orientale S.Kaneko）春孢子多糖的体外抗氧化活性,制备了该菌破壁春孢子精制多糖,并对所得春孢子多糖进行了总抗氧化能力、总还原力以及清除二苯代苦味酰基（DPPH·）、清除羟基自由基（·OH）、清除超氧阴离子（O₂^·）的活性进行了测定。体外抗氧化活性分析结果表明：松栎柱锈菌春孢子多糖具有较强的总抗氧化能力;虽然该菌多糖不具有清除多数氧自由基母体（O₂^·）的作用,也不具有清除人工合成自由基DPPH·的作用,但是其能够有效清除对机体破坏力最强的自由基·OH。这表明本文获得的松栎柱锈菌春孢子多糖具有对自由基选择性清除的能力,对其他自由基研究者具有参考价值,可为该菌的开发利用提供参考,也能够为森林有害生物开发利用提供理论依据。     

Iron (III) Stimulation of Lipid Hydroperoxide-Dependent Lipid Peroxidation

In an experimental system where both Fe²⁺ autoxidation and generation of reactive oxygen species is negligible, the effect of FeCl₂ and FeCl₃ on the peroxidation of phosphatidylcholine (PC) liposomes containing different amounts of lipid hydroperoxides (LOOH) was studied; Fe²⁺ oxidation, oxygen consumption and oxidation index of the liposomes were measured. No peroxidation was observed at variable FeCl₂/FeCl₃ ratio when PC liposomes deprived of LOOH by triphenyl-phosphine treatment were utilized. By contrast, LOOH containing liposomes were peroxidized by FeCl₂. The FeCl₂ concentration at which Fe²⁺ oxidation was maximal, defined as critical Fe²⁺ concentration [Fe²⁺]*, depended on the LOOH concentration and not on the amount of PC liposomes in the assay. The LOOH-dependent lipid peroxidation was stimulated by FeCl₃, addition; the oxidized form of the metal increased the average length of radical chains, shifted to higher values the [Fe²⁺]* and shortened the latent period. The iron chelator KSCN exerted effects opposite to those exerted by FeCl₃ addition. The experimental data obtained indicate that the kinetics of LOOH-dependent lipid peroxidation depends on the Fe²⁺/Fe³⁺ ratio at each moment during the time course of lipid peroxidation. The results confirm that exogenously added FeCl₃ does not affect the LOOH-independent but the LOOH-deendent lipid peroxidation; and suggest that the Feg, endogenously generated exerts a major role in the control of the LOOH-dependent lipid peroxidation.     

Antioxidant Action of Benzylisoquinoline Alkaloids

The antioxidant action of a series of benzylisoquinoline alkaloids has been investigated. Laudanosoline, protopapaverine, anonaine, apomorphine, glaucine, boldine, bulbocapnine, tetrahydroberberine and stepholidine produced a dose-dependent inhibition of microsomal lipid peroxidation induced by Fe²⁺/ascorbate, CCl₄/NADPH or by Fe³⁺ADP/NADPH. Apomorphine exerted the highest inhibitory effects in the three systems of induction used, with a potency higher than propyl gallate. Laudanosoline was particularly effective in the first system, while bulbocapnine and anonaine were more potent when CCl₄/NADPH or Fe³⁺ -ADP/NADPH were used as inducers. Laudanosoline, protopapaverine, apomorphine, tetrahydroberberine and stepholidine were also potent inhibitors of nitroblue tetrazolium (NBT) reduction. The presence of a free hydroxyl group or preferably of a catechol group is a feature relevant for inhibition of lipid peroxidation and NBT reduction, nevertheless the antioxidant activity of benzylisoquinoline alkaloids cannot be only ascribed to the formation of phenoxy radicals and other free radical species may be formed during aporphine and tetrahydroprotoberberine oxidation. The influence of this series of compounds on the time course of lipid peroxidation suggests that some of them, like apomorphine and boldine act as chain-breaking antioxidants.     

The Mechanism of Iron (III) Stimulation of Lipid Peroxidation

A study conducted on Fe²⁺ autoxidation showed that its rate was extremely slow at acidic pH values and increased by increasing the pH; it was stimulated by Fe³⁺ addition but the stimulation did not present a maximum at a Fe²⁺/Fe³⁺ ratio approaching 1:1. The species generated during Fe³⁺-catalyzed Fe²⁺ autoxidation was able to oxidize deoxyribose; the increased Fe²⁺ oxidation observed at higher pHs was paralleled by increased deoxyribose degradation. The species generated during Fe³⁺-catalyzed Fe²⁺ autoxidation could not initiate lipid peroxidation in phosphatidylcholine liposomes from which lipid hydroperoxides (LOOH) had been removed by treatment with triph-enylphosphine. Neither Fe²⁺ oxidation nor changes in the oxidation index of the liposomes due to lipid peroxidation were observed at pHs where the Fe³⁺ effect on Fe²⁺ autoxidation and on deoxyribose degradation was evident. In our experimental system, a Fe²⁺/Fe³⁺ ratio ranging from 1:3 to 2:1 was unable to initiate lipid peroxidation in LOOH-free phosphatidylcholine liposomes. By contrast Fe³⁺ stimulated the peroxidation of liposomes where increasing amounts of cumene hydroperoxide were incorporated. These results argue against the participation of Fe³⁺ in the initiation of LOOH-independent lipid peroxidation and suggest its possible involvement in LOOH-dependent lipid peroxidation.