地鳖多糖提取物的体内外抗氧化作用

目的研究地鳖多糖提取物体内外抗氧化作用。方法体外试验采用分光光度法、邻苯三酚自氧化法和Fe2+-邻二氮菲法分别检测地鳖多糖对二苯代苦味酰基自由基(DPPH·)、超氧阴离子自由基(O-2·)和羟自由基(·OH)的清除,检测体外红细胞氧化溶血和肝线粒体肿胀程度。体内试验小鼠连续灌胃不同剂量(0、40、80、160 mg/kg)地鳖多糖提取物20 d,硫代巴比妥酸(TBA)比色法测定小鼠组织中丙二醛(MDA)含量,分光光度法检测抗氧化酶(SOD、CAT、GSH-Px)活力。结果与对照组比较,地鳖多糖组对自由基清除率随多糖浓度升高而显著提高;体外红细胞氧化溶血和线粒体肿胀显著降低。多糖组小鼠肝肾中MDA含量降低,SOD、CAT、GSH-Px抗氧化酶活力提高并明显高于对照组。结论地鳖多糖提取物能够清除自由基,降低自由基引起细胞氧化损伤,抑制组织中过氧化物生成,提高抗氧化酶活力,具有显著的体内外抗氧化作用。     

松果菊苷抗衰老作用机理研究

研究了中国传统药物肉苁蓉提取物松果菊苷(echinacoside,ECH)体外清除活性氧自由基和体内抗氧化、抗衰老作用的机理。运用电子顺磁共振(electron paramagretic resonance,EPR)自旋捕捉方法研究ECH对体外产生的羟自由基(^ OH)、超氧阴离子自由基(O2^-)和脂自由基(L^ )的清除能力;并以D-半乳糖衰老小鼠为实验模型,采用低温EPR技术直接检测小鼠心、肝、肾、脑组织活性氧物种(reactive oxygen species,ROS)水平;生化方法检测小鼠全血谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)和脑组织单胺氧化酶(monoaminoxidase,MAO)活性及肝组织丙二醛(malondialdehvde,MDA)含量;EPR自旋捕捉方法检测血清超氧化物歧化酶(supemxide dismutase,SOD)活力;跳台法检测小鼠记忆力。结果表明ECH能较好抑制体外^ OH,O2^-和L^ 自由基,同时能够提高GSH-Px和SOD活性,降低MDA含量,因此对D-半乳糖所致衰老引起的活性氧自由基损伤具有一定修复作用。由于抑制了MAO活性而提高小鼠的记忆力。由此可以认为ECH抗脂质过氧化及改善衰老的作用与其抗氧化活性有关。     

魔芋葡甘低聚糖抗氧化性初步研究

为了检验魔芋葡甘低聚糖抗氧化功能,本文测定了魔芋葡甘低聚糖体外清除自由基及保护DNA氧化损伤能力,并通过连续两周用不同剂量的魔芋葡甘低聚糖灌胃小鼠,检测其对肝脏和血浆中丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱肝肽过氧化物酶(GSH-PX)活性的影响。研究结果显示:魔芋葡甘低聚糖对超氧阴离子自由基(.O2-)和羟自由基(.OH)有较好的清除能力,能有效地保护DNA免受羟自由基的损伤,并且能有效地降低肝脏中丙二醛水平,提高肝脏和血浆中SOD、GSH-PX的活性。     

甘草提取物对鼠肝线粒体氧化损伤的保护作用

用60%乙醇回流甘草,得粗提物(RG0),经AB-8大孔树脂纯化RG0得到甘草精提物(RG1),并对RG0和RG1主要活性成分的含量进行测定。为研究RG0和RG1对鼠肝线粒体氧化损伤的保护作用,用Vc-Fe2+诱导线粒体损伤,测定RG0和RG1对ATP酶的活性、线粒体肿胀度和蛋白质羰基含量的影响;用H2O2-Fe2+体系诱导线粒体脂质过氧化,测定RG0和RG1对丙三醛(MDA)含量的影响;用NBT法测定RG0和RG1抑制线粒体产生超氧阴离子的作用。结果显示:RG0和RG1可以显著地抑制线粒体的氧化损伤,并能防止线粒体肿胀和ATP酶活力下降,降低蛋白质羰基化水平,以及具有有效清除线粒体产生的超氧阴离子自由基的作用。因此,RG0和RG1对鼠肝线粒体的氧化损伤具有良好的保护作用,RG1的作用比RG0好。     

肾茶提取物抗氧化及保护线粒体作用研究(英文)

肾茶水提液依次用石油醚、氯仿、乙酸乙酯萃取,与水层得到4个不同极性部位。以清除DPPH·、超氧阴离子和羟自由基的能力,络合Fe2+能力,体外抗活性氧能力以及对FeSO4和H2O2诱导小鼠肾脏组织匀浆脂质过氧化产物MDA和GSH-Px水平的影响,综合评价其抗氧化活性;以抑制Fe2+-L-Cys诱导肾脏线粒体肿胀能力,初步评价其保护肾脏线粒体的作用。结果显示肾茶水提液4个不同极性部位均具有不同程度的清除DPPH·、O-·2、·OH和络合Fe2+能力;其中乙酸乙酯和水提部位具有显著体外抗ROS能力,降低MDA和升高GSHPx水平,以及抑制肾脏线粒体肿胀的能力,且其作用效果均与剂量呈正相关。本实验结果可为肾茶用于治疗肾脏疾病的药效物质基础研究提供依据。     

橙皮苷对小鼠抗氧化作用及抗氧化酶基因表达的影响

目的探讨橙皮苷(HDN)对机体抗氧化作用的影响。方法采用分光光度法、邻苯三酚自氧化法和Fe2+-邻二氮菲法检测HDN体外清除自由基、抑制线粒体肿胀和红细胞氧化溶血;实验小鼠灌服不同浓度HDN(0、80、160、320 mg/kg)连续12 d,ELISA和分光光度法检测小鼠组织中MDA含量,抗氧化酶(SOD、CAT、GSH-PX)活力,RT-PCR技术分析抗氧化物酶mRNA表达水平。结果与对照组比较,HDN组自由基(·OH、O2-·、DPPH·)清除率明显提高,小鼠红细胞体外氧化溶血和线粒体肿胀显著降低;小鼠组织及血清中MDA含量降低,抗氧化酶SOD、CAT、GSH-PX活力明显高于对照组,组织中抗氧化酶mRNA(SOD、CAT、GSH-PX)表达上调。结论 HDN能够清除自由基,降低自由基引起的细胞氧化损伤,抑制过氧化物生成,上调抗氧化酶基因表达及提高酶活力,呈现良好的抗氧化作用。     

连翘叶黄酮的体外抗氧化作用

为研究连翘叶黄酮(Forsythia suspenseleaves flavonoids,FLF)的体外抗氧化作用,用水杨酸法研究FLF清除.OH的效果,并测定了FLF对连苯三酚自氧化体系的抑制作用。用硫代巴比妥酸(TBA)法测定了小鼠4种器官及肝线粒体、微粒体中的丙二醛(MDA)含量,用分光光度法测定了小鼠红细胞溶血和肝线粒体膨胀程度。结果表明,FLF可以清除.OH,抑制连苯三酚自氧化,并抑制.OH所致丙二醛的产生,减少红细胞溶血,减轻肝线粒体膨胀程度。说明FLF具有明显的抗氧化活性。     

香菇多糖对糖尿病大鼠膈肌线粒体的保护作用

目的：研究香菇多糖（LNT）对糖尿病大鼠膈肌线粒体的保护作用。方法：用光镜和电镜观察LNT对糖尿病大鼠膈肌的形态学改变,并测定膈肌线粒体琥珀酸脱氢酶（SDH）、超氧化物歧化酶（SOD）、一氧化氮合酶（NOS）的活性,丙二醛（MDA）、一氧化氮（NO）的含量。结果：LNT治疗后膈肌线粒体病变明显减轻,膈肌线粒体SDH、SOD活性升高,NOS活性及NO、MDA含量下降。结论：LNT能减轻自由基和过量一氧化氮对膈肌线粒体的损伤,从而对糖尿病大鼠膈肌起到保护作用。     

禹州漏芦醇提物对四氯化碳所致小鼠急性肝损伤的影响

探讨禹州漏芦乙醇提取物对四氯化碳(CCl4)诱导小鼠急性肝损伤的保护作用。以CCl4诱导小鼠急性肝损伤模型,检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)活性,同时测定肝匀浆中的超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性和丙二醛(MDA)的水平。将肝大叶HE染色,观察各组小鼠的肝组织病理改变。结果表明,同模型组比较,禹州漏芦乙醇提取物各剂量组均能降低小鼠血清中ALT、AST及MDA活性,升高肝组织中GSH-Px和SOD的活性,并能明显改善肝组织的病理学损伤。禹州漏芦乙醇提取物对CCl4所致小鼠急性肝损伤具有较好保肝作用,其作用可能与清除体内自由基和抗氧化的作用有关。     

绞股蓝提取物对小鼠运动能力的影响

目的：研究绞股蓝提取物对小鼠运动能力的影响。方法：建立动物训练实验模型,测定小鼠肝组织的超氧化物歧化酶（SOD）的活性、丙二醛（MDA）的活性。结果：灌服海南野生绞股蓝提取液后,服药组小鼠肝组织SOD活性显著高于各自对照组．MDA含量显著低于各自对照组。结论：海南野生绞股蓝具有较强的抗脂质过氧化损伤的作用,服用其绞股蓝可消除运动过程中产生过量自由基,保护心脏、肝脏免受自由基的损伤,对肝脏和心肌组织具有显著的保护作用。     

Antioxidant activity of two dibenzocyclooctene lignans on the aged and ischemic brain in rats.

The effects of two dibenzocyclooctene lignans on peroxidative damage of aging and ischemic rat brain were studied. Incubation of eight-month-old rat brain mitochondria and membrane suspension with Fe(2+)-cysteine resulted in the formation of malondialdehyde (MDA) and decrease of ATPase activity. Schisanhenol (Sal) (10(-4) M) completely inhibited the peroxidative damages of brain mitochondria and membrane of rats. The swelling and disintegration of brain mitochondria, as well as the reduction of brain membrane fluidity induced by Fe(2+)-cysteine were also prevented by Sal. The results of imitative experiment of ischemia and reperfusion of brain mitochondria and membrane in vitro indicated that Sal significantly impeded production of MDA and loss of ATPase activity induced by reoxygenation following anoxia. Oral administration of Sal induced increase of cytosol glutathione-peroxidase of brain in mice under the condition of reoxygenation following anoxia. The other compound schizandrin (Sin B) also has similar activity. But its potency is weaker than that of Sal. All these results indicate that Sal and Sin B have protective action against oxidative stress.     

α-生育酚对脑皮层神经元线粒体的保护作用

目的探讨α-生育酚对神经元线粒体的保护作用。方法将神经元细胞进行分组,分为：（1）正常对照组,（2）单纯氧自由基损伤组,（3）α-生育酚保护组。利用Fenton反应造成神经元细胞氧自由基损伤,用激光共聚焦显微镜观察各组神经元JC-1染色结果,并检测各组神经元琥珀酸脱氢酶（SDH）和细胞色素氧化酶（CCO）活性。结果（1）JC-1染色结果分析：α-生育酚保护组神经元线粒体功能强于单纯氧自由基损伤组。（2）SDH和CCO酶活性分析：α-生育酚保护组神经元SDH和CCO酶活性高于单纯氧自由基损伤组。结论α-生育酚可以有效对抗氧自由基对神经元线粒体的损伤。     

Size Effects on the Interaction of QDs with the Mitochondrial Membrane In Vitro

The mitochondrial toxicity induced by GSH-CdTe Quantum dots (QDs) of different sizes was investigated. The decreases in absorbance and transmission electron microscopy images show that QDs induce the swelling of mitochondria. Results of flow cytometry indicate that QDs cause a reduction of mitochondrial membrane potential (MMP). A remarkable increase in fluidity of protein regions of mitochondrial membrane is observed, whereas the lipid regions are not obviously affected. Cyclosporin A (CsA) effectively prevents the QD-induced mitochondrial swelling. On the basis of these results, it is proposed that QDs induce mitochondrial permeability transition (MPT). Moreover, with increasing QDs size, a pronounced MPT is observed. The difference between the membrane fluidity induced by QDs and Cadmium ion and the ineffective protective effects of EDTA suggests that the mitochondrial toxicity of QDs cannot be only attributed to the release of metal ion. The protective effects of HSA indicate that the interaction of QDs with pore-forming protein gives rise to the increase in membrane fluidity. This hypothesis is demonstrated by the interaction of QDs with model membranes and proteins using differential scanning calorimetry and isothermal titration microcalorimetry. In conclusion, as the size of QDs increases, the binding affinity of QDs with membrane protein increases, and therefore causes a pronounced mitochondrial damage.     

Propofol Prevents Oxidative Stress by Decreasing the Ischemic Accumulation of Succinate in Focal Cerebral Ischemia–Reperfusion Injury

Oxidative stress caused by mitochondrial dysfunction during reperfusion is a key pathogenic mechanism in cerebral ischemia–reperfusion (IR) injury. Propofol (2,6-diisopropylphenol) has been proven to attenuate mitochondrial dysfunction and reperfusion injury. The current study reveals that propofol decreases oxidative stress injury by preventing succinate accumulation in focal cerebral IR injury. We evaluated whether propofol could attenuate ischemic accumulation of succinate in transient middle cerebral artery occlusion in vivo. By isolating mitochondria from cortical tissue, we also examined the in vitro effects of propofol on succinate dehydrogenase (SDH) activity and various mitochondrial bioenergetic parameters related to oxidative stress injury, such as the production of reactive oxidative species, membrane potential, Ca²⁺-induced mitochondrial swelling, and morphology via electron microscopy. Propofol significantly decreased the ischemic accumulation of succinate by inhibiting SDH activity and inhibited the oxidation of succinate in mitochondria. Propofol can decrease membrane potential in normal mitochondria but not in ischemic mitochondria. Propofol prevents Ca²⁺-induced mitochondrial swelling and ultrastructural changes to mitochondria. The protective effect of propofol appears to act, at least in part, by limiting oxidative stress injury by preventing the ischemic accumulation of succinate.     

Enterocyte mitochondrial dysfunction due to oxidative stress

The endogenous production of H2O2 in isolated rat intestinal mitochondria and oxidant induced damage to mitochondria were examined. There was an appreciable amount of H2O2 production in presence of succinate, glutamate and pyruvate, while the presence of rotenone with succinate further increased production. Superoxide generated by the X-XO system induced membrane permeability transition (MPT), calcium influx, lipid peroxidation and changes in membrane fluidity in mitochondria. A decreased mitochondrial ATPase activity and uncoupling of respiration was also observed. Spermine inhibited swelling induced by X-XO and also blocked the calcium influx and reversed the membrane fluidity changes.     

5-methoxytryptophol preserves hepatic microsomal membrane fluidity during oxidative stress

Lipid peroxidation is a degenerative chain reaction in biological membranes that may be initiated by exposure to free radicals. This process is associated with changes in the membrane fluidity and loss of several cell membrane-dependent functions. 5-methoxytryptophol (ML) is an indole isolated from the mammalian pineal gland. The purpose of this study was to investigate the effects of ML (0. 01mM-10mM) on membrane fluidity modulated by lipid peroxidation. Hepatic microsomes obtained from rats were incubated with or without ML (0.01-10 mM). Then lipid peroxidation was induced by FeCl(3), ADP, and NADPH. Membrane fluidity was determined using fluorescence spectroscopy. Malonaldehyde (MDA) +4-hydroxyalkenals (4-HDA) concentrations were estimated as an indicator of the degree of lipid peroxidation. With oxidative stress, membrane fluidity decreased and MDA+4-HDA levels increased. ML (0.01-3 mM) reduced membrane rigidity and the rise in MDA+4-HDA formation in a concentration-dependent manner. 10 mM ML protected against lipid peroxidation but failed to prevent the membrane rigidity. In the absence of oxidative reagents, ML (0.3-10 mM) decreased membrane fluidity whereas MDA+4-HDA levels remained unchanged. This indicates that ML may interact with membrane lipids. The results presented here suggest that ML may be another pineal indoleamine (in addition to melatonin) that resists membrane rigidity due to lipid peroxidation.     

丙二醛对离体草鱼肠道黏膜细胞的损伤作用

以丙二醛为实验材料, 在草鱼Ctenopharyngodon idella肠道黏膜细胞培养液中加入不同浓度丙二醛, 研究丙二醛不同剂量、不同作用时间下对肠道黏膜细胞生长、细胞形态结构及相关酶活性的变化. 结果显示: 添加(1.23-9.89) mol/L丙二醛在3-9h时显著抑制了离体草鱼肠道黏膜细胞生长及存活率, 以6h时抑制程度较为明显, 导致贴壁细胞减少, 细胞集落面积减小, 其中添加4.94 mol/L丙二醛细胞胞浆内脂肪滴沉积, 空泡变性, 同时线粒体肿胀, 核固缩; 丙二醛对细胞分化成熟有抑制, 且增加细胞器膜的通透性, 导致胞浆酶漏出; 6h时丙二醛处理组培养液中GSH-PX、T-AOC活力显著降低(P0.05). 结果表明: 添加(1.23-9.89) mol/L丙二醛对草鱼肠道黏膜细胞产生了损伤, 表现为抑制细胞生长, 改变细胞形态、结构, 导致膜结构破坏, 且作用程度与添加浓度、作用时间呈正相关关系. 研究认为丙二醛对草鱼肠道黏膜细胞具有显著性的损伤作用.       

谷胱甘肽的抗线粒体脂质过氧化作用

谷胱甘肽是细胞内重要的抗氧化损伤物质之一．以NADH诱导的牛心肌线粒体脂质过氧化体系为模型,研究了谷胱甘肽的抗氧化作用．结果表明,一定浓度的谷胱甘肽能够部分抑制该体系中线粒体的脂质过氧化．保护组的丙二醛含量为损伤组72．5％;线粒体的膨胀度较损伤组降低;细胞色素C氧化酶及ATP酶活力分别较损伤组提高了1．5及2．2倍．     

支链氨基酸对心肌缺血大鼠线粒体损伤的保护作用

目的和方法：本文用异丙肾上腺素（Ｉｓｏ） 造成大鼠心肌缺血动物模型,观察支链氨基酸（ＢＣＡＡ）对大鼠心肌缺血时线粒体结构和功能损伤的预防作用。结果：ＢＣＡＡ 能显著降低心肌缺血后心肌线粒体中丙二醛（ＭＤＡ） 水平、维持线粒体模平均微粘度（－η） 、线粒体呼吸链中细胞色素氧化酶及心肌肌球蛋白ＡＴＰａｓｅ活力。结论：给予ＢＣＡＡ对保护大鼠心肌线粒体的结构和功能免受缺血性损伤具有一定效果     

水分胁迫对甘蔗叶片线粒体膜流动性的影响及其与膜脂过氧化的关系

用荧光探剂ANS对抗旱性不同的甘蔗品种在水分胁迫下叶片线粒体膜流动性的变化进行的研究表明,水分胁迫降低了线粒体膜的流动性,抗旱性强的甘蔗品种Co 617和F.Y.79-9的下降幅度分别小于抗旱性弱的Co 740和M.T.77-208;水分胁迫下线粒体膜流动性的下降与膜脂过氧化产物丙二醛含量的增加有密切关系。外源自由基处理试验也表明,甘蔗叶片线粒体膜流动性的下降与膜脂过氧化作用有关。