安吉白茶黄酮抗氧化活性的体外实验研究

目的通过研究安吉白茶黄酮对自由基的清除作用及抗脂质过氧化作用来系统阐明安吉白茶黄酮的抗氧化活性。方法应用化学发光法和分光光度法系统评价了安吉白茶黄酮对超氧阴离子自由基(O-2·)、羟基自由基(·OH)、二苯代苦味酰基自由基(DPPH·)和H2O2的清除作用。采用小鼠肝脏为研究对象,评价了安吉白茶黄酮对自发及诱导性脂质过氧化模型的抑制作用。结果安吉白茶黄酮对O-2·、·OH、DPPH·和H2O2均有较强的清除能力,其清除作用与黄酮浓度呈明显的剂量依赖关系。安吉白茶黄酮可以以剂量依赖方式抑制小鼠肝脏脂质过氧化。结论安吉白茶黄酮在体外具有高效的自由基清除作用,并具有较强的抗脂质过氧化活性。     

当归内酯清除自由基及抗氧化活性的研究

目的 研究当归内酯清除自由基和抗氧化活性的作用.方法 采用体外实验研究当归内酯对1-1-二苯基苦基苯肼自由基(DPPH·)和·OH的清除作用,自身还原能力的强弱,以及对亚油酸和H2O2诱导的红细胞膜脂质过氧化的保护作用.结果 当归内酯对DPPH·和·OH具有良好的清除作用,其IC50分别为2.0、7.6 mg·mL-1;1、4、16 mg·mL-1的当归内酯对亚油酸的自发氧化和H2O2诱导的红细胞氧化溶血均表现出一定的抑制作用,且呈一定的量效关系.此外,各浓度梯度的当归内酯均具有一定的还原能力.结论 当归内酯具有清除自由基和抗氧化的作用.     

复方免疫散多糖及其拆方的体外抗氧化作用

目的 研究复方免疫散多糖及其拆方的体外抗氧化作用.方法 测定3种多糖对·OH、DPPH·、超氧阴离子自由基的清除能力,用硫代巴比妥酸法测定其对脂质过氧化的抑制作用以及金属离子的螯合,评价复方免疫散多糖及其拆方的抗氧化活性.结果 复方免疫散多糖及其拆方呈剂量依赖性地清除·OH、DPPH、超氧阴离子自由基,抑制脂质过氧化及螫合金属离子.结论 复方免疫散多糖及其拆方在体外具有抗氧化能力.     

冬凌草多糖的提取、分离及抗氧化活性研究

目的研究冬凌草多糖的性质及抗氧化活性。方法冬凌草经过热水、稀碱提取,乙醇沉淀得到冬凌草粗多糖,进一步纯化后得到两个主要组分命名为ST和JT,通过高效液相色谱法对其单糖组成、纯度及分子质量进行了测定,并通过清除二苯代苦味酰肼(DPPH)自由基、羟基自由基、超氧阴离子自由基和抗脂质过氧化能力等体外实验,考察了ST和JT的体外抗氧化活性。结果 ST中主要含有D-半乳糖(Gal)、D-甘露糖(Man)、D-(+)-半乳糖醛酸(GalUA)和D-木糖(Xyl)四种单糖,JT中主要含有Xyl、L-鼠李糖(Rha)、Gal和D-葡萄糖醛酸(GlcUA)四种单糖,ST和JT纯度均较高,分子质量分别约为39 100和26 200。ST和JT对DPPH自由基和羟基自由基均有较强的清除能力,且均没有清除超氧阴离子自由基和抗脂质过氧化能力。结论冬凌草多糖为复杂的杂聚多糖,且具有一定的抗氧化活性。     

老龙皮多糖及水提物体外抗氧化活性比较

摘 要 目的：比较老龙皮水提物及老龙皮多糖的体外抗氧化活性。方法: 在体外化学模拟的条件下,采用比色法测定并比较老龙皮多糖及老龙皮水提物对Fe3+的还原能力,对羟基自由基、DPPH自由基、超氧阴离子自由基的清除能力以及对脂质过氧化的影响。结果: 老龙皮多糖及水提物能还原Fe3+,清除DPPH自由基及抗脂质过氧化反应,且老龙皮多糖优于水提物(P<0.05);同时两者还具有清除羟基自由基及超氧阴离子的作用,老龙皮多糖优于水提物,两者差异无统计学意义(P>0.05)。结论: 老龙皮多糖以及水提物具有一定的体外抗氧化活性,且老龙皮多糖的抗氧化活性优于老龙皮水提物,老龙皮多糖为老龙皮主要活性物质。     

藏药波棱瓜子提取物对肝损伤大鼠的抗氧化作用

目的考察波棱瓜子提取物的抗氧化作用及其自由基清除活性。方法体内实验采用CCl4损伤肝脏引起大鼠脂质过氧化反应,测定肝细胞中的丙二醛(MDA)、抗氧化酶(SOD、GSH-px)的含量。体外实验采用DPPH自由基清除法。结果波棱瓜子的CHCl3提取物具有较强的清除DPPH自由基的能力,IC50为49.69μg.ml-1,活性与阳性对照VitE相当。连续给波棱瓜子提取物7 d,能显著改善CCl4引起的肝细胞损伤。波棱瓜子的CHCl3及水提取物均能显著抑制由CCl4引起的脂质过氧化,使MDA的含量显著下降,能不同程度提高肝细胞中SOD、GSH-px的活性。结论波棱瓜子提取物具有较强的抗氧化活性,且有较强的自由基清除活性。这可能是波棱瓜子能清热解毒、用于治疗"赤巴"病的作用机理之一。     

红曲霉菌对姜黄素的转化及产物自由基清除和抗脂质过氧化作用的研究

目的研究红曲霉菌对姜黄素的微生物转化及转化总产物的自由基清除和抗脂质过氧化的作用,并对转化产物进行了初步分析。方法用本实验室保存的红曲霉菌对姜黄素进行微生物转化,同时设立菌株对照和底物对照;研究转化总产物对DPPH自由基的清除能力;研究转化总产物对食饵性高脂血症小鼠肝脏和血清MDA、SOD、GSH—Px等过氧化脂质的影响。用乙酸乙酯提取转化产物,用TLC、HPLC—DAD（Agilent Zorbax Extend C18柱,0．1％乙酸和乙腈梯度洗脱,流速1．0mL-min^-1）对转化产物进行了初步分析。结果姜黄素转化总产物在10000～400mg·mL^-1（相当于含姜黄素100～4 mg·mL^-1）内有很强的自由基清除能力,总产物浓度在100mg·mL^-1还保留了47．46％的清除能力;而底物对照物在10000、2000mg·mL^-1时有一定的清除能力,但浓度在400mg-mL^-1时自由基清除能力已明显减弱,100mg-mL^-1以下已基本消失。转化总产物500,200,100mg·kg·d^-1（相当于姜黄素5,2,1mg·kg·d^-1）均能降低高脂血症小鼠肝脏和血清的过氧化脂质,而菌株对照组（500mg·kg·d^-1）和底物对照组（500mg·kg·d^-1,相当于姜黄素5mg·kg·d^-1）抗脂质过氧化作用不明显。研究超氧化物歧化酶、谷胱甘肽过氧化物酶,发现姜黄素转化产物对此二酶的作用不明显,其抗氧化作用可能并非通过改变此二酶的活性。转化产物经HPLC—DAD分析,发现可能存在6个转化产物,其保留时间分别为16．3,22．1,23．2,28．0,33．0,36．1min,其光谱图与姜黄素存在明显差异。结论姜黄素经红曲霉菌转化后形成了由6个代谢产物组成的新组合型天然姜黄素类似物群,其自由基清除能力和抗脂质过氧化作用显著增强。     

新疆紫草不同极性部位的抗氧化活性研究

目的比较新疆紫草不同极性部位提取物的抗氧化活性。方法采用超临界CO2萃取得到超临界提取物后,萃余物依次用95%乙醇和60%的乙醇提取,对得到的乙醇提取物分别采用不同极性的溶剂分步萃取得到紫草不同极性部位的8个提取物,对上述9个提取物的清除羟基自由基、清除DPPH自由基、总抗氧化活性、抑制脂质过氧化能力等进行了评价。结果超临界CO2萃取物的总抗氧化活性在所有试样中居中,在1 mg·mL 1的浓度下,其清除羟基自由基和DPPH自由基的活性接近或略低于对照品芦丁和BHT,而中等极性部分的乙酸乙酯提取物的抗氧化活性最强,高于同等浓度的对照品BHA和芦丁,但极性较大的部位试样的抗氧化活性总体上相对较弱。结论紫草提取物的各极性部位均具有不同程度的抗氧化能力。     

玳玳果总黄酮体外抗氧化作用的研究

目的探讨玳玳果总黄酮有效部位的抗氧化作用。方法分别采用二苯代苦味酰基自由基法(DPPH.法)、水杨酸法(Fenton反应法)和硫代巴比妥酸法(TBAS法)等方法,进行玳玳果总黄酮有效部位抗氧化药效实验研究,评价玳玳果总黄酮对DPPH.自由基、.OH自由基的清除能力,测定玳玳果总黄酮对小鼠肝脂质过氧化的抑制作用。结果玳玳果总黄酮有效部位对DPPH.自由基及.OH自由基均具有良好的清除作用,其自由基清除能力以半数清除率计分别为0.417 mg.mL1和3.807 mg.mL1,同时对小鼠肝脂质过氧化具有显著的抑制作用,呈良好的量效相关性。结论玳玳果总黄酮有效部位具有良好的抗氧化清除自由基作用。     

蒜氨酸、蒜酶及其混合物的体外抗氧化活性研究

研究蒜氨酸、蒜酶及其混合物的体外抗氧化活性.方法建立超氧阴离子自由基(·O2-)和羟基自由基(·OH)产生体系,应用Fe2+引发的卵磷脂过氧化体系,分别采用羟胺法、水杨酸法及硫代巴比妥酸法测定蒜氨酸、蒜酶及其混合物对·O2 -和·OH的清除能力及抗脂质过氧化能力.结果蒜氨酸,蒜酶及其混合物对·O2 -和·OH具有良好的...     

Tea catechins protect against lead-induced cytotoxicity, lipid peroxidation, and membrane fluidity in HepG2 cells.

Recent studies have shown that lead causes oxidative stress by inducing the generation of reactive oxygen species (ROS) and reducing the antioxidant defense system of cells. This suggests that antioxidants may play an important role in the treatment of lead poisoning as a kind of excellent scavenger of free radicals and chelator of heavy metal. Whether tea catechins have protective effects against oxidative stress after lead treatment in cell systems remains unclear. The present study was designed to elucidate if tea catechins have any protective effects on lipid peroxidation damage in lead-exposed HepG2 cells. Exposure of HepG2 cells to Pb(++) decreased cell viability and stimulated lipid peroxidation of cell membranes as measured by the thioburbituric acid reaction. Electron spin resonance (ESR) spin-labeling studies indicated that lead exposure could decrease the fluidity in the polar surface of cell membranes. Tea catechin treatment significantly increased cell viability, decreased lipid peroxidation levels, and protected cell membrane fluidity in lead-exposed HepG2 cells in a concentration-dependent manner. The galloylated catechins showed a stronger effect than nongalloylated catechins. Cotreatment with (-)-epigallocatechin gallate (EGCG) and (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), and (-)-epigallocatechin gallate (EGCG) showed a synergistically protective effect. The results suggest that tea catechin supplementation may have a role to play in modulating oxidative stress in lead-exposed HepG2 cells.     

The Inhibitory Effect of Tannins on Lipid Peroxidation of Rat Heart Mitochondria

We induced lipid peroxidation in rat heart mitochondria with ferrous sulphate (FeSO₄₎) and compared the inhibitory effect of various tannins on the peroxidation. Oxygen consumption and malondialdehyde (MDA) formation were used to quantitate the amount of lipid peroxidation, and the free radical scavenger activity of tannins was measured with a diphenyl-ρ-picryl hydrazyl (DPPH) method. Of 25 tannins and related compounds tested, catechin benzylthioether and procyanidin B-2 ben-zylthioether were the most potent in inhibiting lipid peroxidation, with inhibitory effects stronger than that of trolox, a water soluble analogue of vitamin E. The concentrations (IC50) required for catechin benzylthioether and procyanidin B-2 benzylthioether to inhibit oxygen consumption to 50% of control values were 0·85 and 2·0 μm, respectively, while their IC50 values from the inhibition of MDA formation were 0·9 and 1·70 μm, respectively. The IC50 values for catechin and procyanidin B-2 to inhibit oxygen consumption were 34·0 and 11·0 μm. Both compounds were less potent than their benzylthioether derivatives. However, the ability of catechin and procyanidin B-2 to scavenge DPPH were similar to that of their benzylthioether derivatives. We conclude that conjugation with a benzylthioether group enhances the inhibitory effect of tannins on lipid peroxidation, and that the mechanism is not an increase in its scavenger activity.     

Hydroxyl radical scavenging action of tinoridine

Radical scavenging action of tinoridine, a non-steroidal anti-inflammatory drug with a potent anti-peroxidative activity, was investigated. Tinoridine reduced a stable free radical, diphenyl-p-picryl-hydrazyl, in the molar ratio of about 1:2, indicating its free radical scavenging ability. Tinoridine inhibited the lipid peroxidation in rat liver microsomes induced by xanthine-xanthine oxidase system in the presence of ADP and Fe2+, in which hydroxyl radical (. OH) is formed. Tinoridine was demonstrated to be oxidized in the course of the lipid peroxidation by following the fluorescence derived from the oxidation product of tinoridine. It was also oxidized by the xanthine-xanthine oxidase system in the presence of Fe2+, but its oxidation was slow in the absence of Fe2+ and almost completely inhibited by catalase. Tinoridine was also oxidized by H2O2-Fe2+ system producing . OH (Fenton reaction), but it did not affect the reduction of cytochrome c caused by superoxide radical. These results indicate that tinoridine is able to scavenge . OH and the main active oxygen species responsible for the lipid peroxidation is . OH. The anti-peroxidative and . OH scavenging ability of tinoridine should contribute to its anti-inflammatory action.     

Comparative study of antioxidant potential of tea with and without additives

Oxidative damage is one of the many mechanism leading to chronic diseases. Therefore interest is growing in the protection afforded by antioxidant nutrients against free radical reactions. More recently, the attention has shifted to polyphenols. Polyphenols are secondary plant metabolites occurring widely in plant food. They possess outstanding antioxidant properties, suggesting a possible protective role in man. Tea (Camellia sinensis) is a widely consumed beverage throughout the world containing polyphenols more than 35% of its dry weight. In the present work we have investigated the effect of tea without milk, tea with milk and lemon tea on the serum lipid peroxidation level (as a parameter of free radical generation). The results show that there were significant decrease in serum lipid peroxidation (Malonaldehyde) level half hour after ingestion of lemon tea and tea without milk which tends to normalize with increase in time. This decrease is much significant in case of lemon tea than tea without milk after half hour or one hour. Hence the interpretation is, tea without milk is a good source of antioxidant and addition of lemon to tea increases its antioxidant potential.     

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     

Studies on membrane factors in iron-supported lipid peroxidation

Lipid peroxidation in biomembranes is mediated by free radical reactions. It leads to membrane damage and has been proposed to be associated with the pathogenesis to tissue injuries. Iron is known as a catalyst of lipid peroxidation. Microsomal lipid peroxidation by both NADPH and iron-chelate, such as Fe(3+)-ADP or Fe(3+)-PPi, is believed to be enzymatically associated with iron reduction. On the other hand, the addition of free Fe2+ to microsomes or liposomes produces a lag phase before the maximal rates of lipid peroxidation. We examined the interaction of iron with membrane in iron-supported lipid peroxidation and microsomal membrane components associated with iron reduction in NADPH-supported lipid peroxidation. Iron-supported lipid peroxidation was affected by the surface charges of liposomal membrane. Liposomes containing phosphatidylserine (PS) were most sensitive to iron-supported lipid peroxidation. The effect of PS on iron-supported lipid peroxidation indicates that iron participates in binding to membrane surface charges and also indicates that Fe2+ at high level bound to membranes plays a role in producing a lag phase. The mechanism producing a lag phase in Fe(2+)-PPi-supported lipid peroxidation is discussed. In NADPH-supported lipid peroxidation in microsomes, it seemed unlikely that superoxide may be involved in iron reduction. Alternatively, under anaerobic conditions, NADPH-supported iron reduction in microsomes was not dependent on cytochrome P450 content and not inhibited by CO. A cholate-solubilized fraction of microsomes was applied to a laurate-Sepharose column and an active fraction for lipid peroxidation was obtained. Involvement of a heat-labile component, distinct from cytochrome P450, responsible for iron reduction in microsomal lipid peroxidation was demonstrated.     

Hepatoprotective and therapeutic effects of tetramethylpyrazine on acute econazole-induced liver injury

2,3,5,6-Tetramethylpyrazine (TMP) is well known as a true calcium antagonist. The aim of this study was to investigate the hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury. The hepatological effect of various concentrations of TMP was first assessed by the biochemical assays of SGOT and SGPT and then by hepatohistological microscopic examination. The dose-response relationship of liver injury induced by various doses of econazole was observed simultaneously from serum biochemical assay of SGOT and SGPT, and also from hepatohistological microscopic examination, by determination of the hepatoprotective effects of various concentrations of TMP on SGOT and SGPT elevation induced by a hepatotoxic dose of econazole (300 mg/kg). The inhibitory effect of various concentrations of TMP or vitamin E (positive control, 0.5 mM in vitro, 0.69 mM in vivo) on FeCl 2 -induced (in vitro) or econazole-induced (in vivo) lipid peroxidation was also investigated. The superoxide scavenging activity of various concentrations of TMP in econazole-damaged rat liver homogenate was assessed by the cytochrome C reduction method. Results showed that the hepatoprotective effect of TMP might be, at least in part, due to its inhibitory ability on membrane lipid peroxidation and free radical formation, or due to its free radical scavenging ability. Improvement of serum transaminases and MDA levels in rat liver homogenate, hepatohistological microscopic examination, and assessment of free radical scavenging activity by the cytochrome C reduction method were used to detect hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury.     

Inhibition of lipid peroxidation by pindolol

Among beta-blockers, including atenolol, metaproterenol, pindolol and propranolol, only pindolol strongly inhibited lipid peroxidation induced by xanthine oxidase-hypoxanthine in the presence of adenosine-5'-phosphate-Fe3+. In the reaction system, superoxide predominantly reduced iron because superoxide dismutase strongly prevented the iron reduction. However, pindolol had no effect on the superoxide-dependent iron reduction. Adding superoxide dismutase immediately stopped the lipid peroxidation, indicating that superoxide is closely connected with forming the initiator of xanthine oxidase-hypoxanthine-induced lipid peroxidation. On the other hand, pindolol also inhibited lipid peroxidation, whereas it did not react with superoxide, indicating that it inhibited xanthine oxidase-hypoxanthine-induced lipid peroxidation by an independent mechanism of superoxide. Pindolol sharply scavenged 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonate) radical cations, but the ability of pindolol to scavenge peroxyl radicals of 2,2'-azobis(2-amidinopropane)-dihydrochloride and 2,2'-diphenyl-p-picrylhydrazyl radicals was low. In addition, pindolol did not scavenge hydroxyl radicals at physiologically significant concentrations. These results suggest that the ability of pindolol to inhibit lipid peroxidation was due to scavenging carbon-centered radicals rather than peroxyl radicals.     

Effects of baicalein and alpha-tocopherol on lipid peroxidation, free radical scavenging activity and 12-O-tetradecanoylphorbol acetate-induced ear edema.

The effects of baicalein, a flavonoid, and alpha-tocopherol (vitamin E) on lipid peroxidation in rat forebrain homogenates, on free radical scavenging action against diphenyl-p-picrylhydrazyl (DPPH), and on 12-O-tetradecanoylphorbol acetate (TPA)-induced ear edema in mice were studied. Baicalein inhibited lipid peroxidation in forebrain homogenates, DPPH-induced free radical and TPA-induced ear edema as potently as did quercetin and nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, and more potently than BW755C, a mixed cyclooxygenase and lipoxygenase inhibitor. Lipid peroxidation in forebrain homogenates, DPPH-induced free radical and TPA-induced ear edema were also inhibited by alpha-tocopherol. Flavone showed no reaction. These results suggest that lipid peroxidation may play an important role in the pathogenesis of TPA-induced ear edema in mice.     

Effects of alpha-phenyl-N-tert-butyl nitrone and N-acetylcysteine on hydroxyl radical formation and dopamine depletion in the rat striatum produced by d-amphetamine.

Previous studies have shown that treatment with free radical scavengers attenuated the D-amphetamine (AMPH) neurotoxicity. But several of these agents also prevent AMPH-induced elevation of body temperature in the rat. Thus, further studies are needed to determine if blockade of the production of free radical or hypothermia are related to the neuroprotective mechanism of the free radical scavengers for AMPH neurotoxicity. In the present study, we examined the effects of the free radical scavengers alpha-phenyl-N-tert-butyl nitrone (PBN) and N-acetylcysteine (NAC) on long-term depletion of striatal dopamine (DA) and lipid peroxidation formation and on hyperthermia induced by AMPH. We also determined their effects on acute hydroxyl radical formation after direct intrastriatal infusion of AMPH. The results showed that both significantly attenuated long-term DA depletion and lipid peroxidation formation in the rat striatum at the dose range that did not block hyperthermia induced by AMPH. These agents also completely inhibited the production of hydroxyl radical after AMPH infusion into the striatum. Our results suggest that free radical scavengers such as PBN and NAC could protect against AMPH-induced oxidative stress and DAergic terminal toxicity via their free radical removing property independent of lowering the core body temperature of rats, and imply that supplement with antioxidants is a potential strategy in the treatment of AMPH neurotoxicity.