Antioxidant Properties of Sulfinates: Protective Effect of Hypotaurine on Peroxynitrite-Dependent Damage

It has been proposed that hypotaurine may function as an antioxidant in vivo. We investigated whether this compound can act as protective agent able to prevent damage from peroxynitrite, a strong oxidizing and nitrating agent that reacts with several biomolecules. The results showed that the compound efficiently protects tyrosine against nitration, alpha1-antiproteinase against inactivation, and human low-density lipoprotein against modification by peroxynitrite. Hypotaurine is also highly effective in inhibiting peroxynitrite-mediated nitration of tyrosine in the presence of added bicarbonate. This result suggests that hypotaurine could play an important role as protective agent under physiological conditions. Moreover, it was found that cysteine sulfinic acid, but not taurine, possesses protective properties against peroxynitrite-dependent damage similar to hypotaurine. These findings indicate that the protective effects exerted by these compounds may be attributable to the presence of the sulfinic group oxidizable into sulfonate by scavenging peroxynitrite and/or its derived species.     

Thiourea and Dimethylthiourea Inhibit Peroxynitrite-Dependent Damage: Nonspecificity as Hydroxyl Radical Scavengers

Thiourea and, more recently, dimethylthiourea, have been used as hydroxyl radical (OH√) scavengers in experiments both in vitro and in vivo. We show that both compounds can inhibit nitration of the amino acid tyrosine on addition of peroxynitrite, and also the inactivation of -antiproteinase by peroxynitrite. Hence, protective effects of (dimethyl) thiourea could be due to inhibition of peroxynitrite-dependent damage as well as to OH√ scavenging, and these compounds must not be regarded as specific OH√ scavengers. © 1997 Elsevier Science Inc.     

谷氨酰胺防治辐射损伤的作用

综述了谷氨酰胺 (Gln)对辐射损伤的防护作用。重点介绍了Gln对辐射引起的肠道损伤、免疫功能和细胞损伤的防护作用 ,并介绍了Gln在肿瘤放射中的作用     

Antioxidant and Antimicrobial Activity in Some Indian Herbal Plants: Protective Effect against Free Radical Mediated DNA Damage

Indian herbal plant species Lantana indica, Adhatoda vasica, Pandanus furcatus, Tylophora indica and Centella asiatica, traditionally used in ethno medicines to treat common infections and various disorders, have been studied for their antimicrobial and antioxidant activity. The methanolic extracts of the plant leaves exhibited significant and dose-dependent antioxidant activities in DPPH radical scavenging, ferric ion reducing and phosphomolybdate assays. These leaf extracts showed antimicrobial activity against selected Gram +ve and Gram ?ve bacterial strains. A. vasica and L. indica extracts possessed maximum antioxidant and antimicrobial activity, respectively. The activities could be correlated to phenolics and flavonoid content of the leaf extracts which ranged from 30.25 to 91.98 mg GAE g^?1 dw leaf extract and 2.67 to 96.45 mg RE g^?1 dw leaf extract respectively. The aqueous extracts of plant leaves significantly protected the DNA damage against the oxidative damage caused by hydroxyl radicals.     

银杏内酯B 对星形胶质细胞氧化损伤的保护作用

目的:探讨银杏内酯B对过氧化氢(H_2O_2)诱导的星形胶质细胞损伤的保护作用及可能机制。方法:星形胶质细胞传代培养,分为阴性对照组(以正常培养液培养),氧化损伤组(100μmol·L~(-1)的H_2O_2作用12 h),银杏内酯B低剂量组(1×10~(-6) mol·L~(-1)银杏内酯B孵育24 h后,加入H_2O_2作用12 h)和银杏内酯B高剂量组(1×10~(-4) mol·L~(-1)银杏内酯B孵育24 h后,加入H_2O_2作用12 h),MTT比色法检测细胞存活率,流式细胞仪检测细胞活性氧(ROS)水平,分光光度计检测上清液中超氧化物歧化酶(SOD)、如谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)的含量。结果:银杏内酯B能抑制氧化损伤引起的细胞活性的下降,降低星形胶质细胞内ROS的生成,促进SOD、GSH-Px水平的升高及MDA水平的下降。结论:银杏内酯B通过提高细胞内SOD、GSH-Px含量,降低细胞内MDA含量发挥其较强的抗氧化作用,从而为其用于治疗神经系统疾病提供可靠的实验依据。     

茶多糖的抗氧化活性及对细胞氧化损伤的保护机制

茶多糖是一种从茶叶中提取的酸性糖蛋白,具有良好的抗氧化活性。以自由基清除率为指标,分析皖西南地区夏秋茶多糖的抗氧化活性,基于H₂O₂和EDTA-Fe²⁺建立的外源性羟基自由基(·OH)损伤细胞模型和PMA诱导内源性羟基自由基损伤模型,进一步探讨茶多糖对自由基损伤的修复作用机制。结果表明,茶多糖具有良好的体外抗氧化活性,对DPPH·和·OH均具有较强的清除效果,EC₅₀值分别为209.5和535.2μg·mL^–1,最大清除效率与Vc相当。细胞增殖实验表明,外源性和内源性自由基氧化损伤模型中细胞存活率均随着茶多糖浓度的增加而升高,在茶多糖浓度为800μg·mL^–1时细胞存活率分别高达87.41%和85.84%,且显著高于模型组(47.67%和48.03%)。在修复机制上,利用激光共聚焦显微镜显影细胞内活性氧(ROS)分布以及荧光强度,分析结果显示,与模型组相比,茶多糖对于细胞模型中外源和内源性ROS均具有明显的清除效果,与体外抗氧化实验结果一致。茶多糖在体外表...     

染料木黄酮改善γ射线损伤小鼠抗氧化功能的作用

用137Csγ射线照射雄性昆明小鼠,观察饲料中补充染料木黄酮(Genistein,Gen)对抗氧化功能的保护作用,探讨其抗辐射作用的机制。结果表明,Gen可以提高辐射小鼠脾和胸腺组织总抗氧化能力(T-AOC)、降低血清、肝脏和胸腺组织丙二醛(MDA)水平;显著提高辐射小鼠抗氧化功能。     

Hypotaurine disproportionation reaction: Identification of products

Summary Hypotaurine, concentrated under reduced pressure in HCl solution, partially (30–40%) degrades into taurine (about 30%), 2-aminoethyl-2-aminoethanethiolsulfonate (about 10%) and ethanolamine. The degradation products were identified using LC/APCI-MS, NMR, amino acid analysis and various chromatographics. The identities were confirmed by comparing the HPLS, MS and NMR characteristics of authentic compounds. One of the degradation processes during concentration of HCl solution of hypotaurine is therefore a disproportionation reaction which can interfere with the experimental results, when studying hypotaurine in biological systems.Abbreviations LC/APCI-MS liquid chromatography/atmospheric pressure chemical ionization-mass spectrometry - TLC thin layer chromatography - DTNB 5,5-dithiobis(2-nitrobenzoic acid)     

白藜芦醇预处理对人鼠脑缺血再灌损伤的保护作用

目的:探讨白藜芦醇预处理对大鼠脑缺血再灌损伤的保护作用及其分子机制.方法:大鼠随机分成假手术组、缺血溶剂组、白藜芦醇预处理组,四动脉阻塞(4-VO)法建立前脑缺血模型,缺血10min/再灌22h,试剂盒检测大鼠海马组织SOD活力及NO、MDA含量变化,RT-PCR法观察GRP78 mRNA的表达.结果:缺血溶剂组海马组织SOD活性明显低于假手术组,NO、MDA含量高于假手术组;缺血前白藜芦醇预处理能显著反转缺血诱导的SOD活力和NO、MDA水平变化,脑缺血能明显上调GRP78 mRNA水平;白藜芦醇预处理能有效抑制缺血诱导的GRP78表达,与缺血组比有显著性差异.结论:白藜芦醇能通过上调SOD活力,减少NO、MDA的生成来抑制缺血后自由基的生成和积累,继而缓解内质网应激、下调GRP78的表达,减轻缺血性脑组织损伤.     

海兔素对刀豆蛋白A诱导的化学性肝损伤保护作用

目的:探讨海兔素对刀豆蛋白A诱导的化学性肝损伤保护作用。方法:雄性Wistar大鼠随机分为4组。模型组与海兔素组给予15 mg/kg刀豆蛋白A尾静脉注射每周一次,制作化学性肝损伤模型,模型制作成功后,正常对照组、模型组每日给予大豆油灌胃,海兔素低、高剂量组给予100、150 mg/kg·d海兔素+大豆油灌胃。实验持续8周后,禁食12 h,处死大鼠。HE染色观察肝组织形态学改变;Masson Trichrome及天狼星红染色观察肝组织纤维化状况;全自动生化分析仪检测血清ALT、AST及LDH水平;ELISA实验测定血清TNF-α和TGF-β1水平。结果:与正常对照组相比,模型组大鼠肝小叶结构模糊紊乱,纤维组织增生明显,可见灶状坏死及炎性细胞浸润,胶原纤维明显增多,胶原指数明显升高。血清中ALT、AST、LDH及TNF-α和TGF-β1水平显著升高(P0.05)。海兔素干预后,肝小叶病变程度较模型组明显减轻,染色胶原显著减少,纤维增生明显改善,血清中ALT、AST、LDH及TNF-α和TGF-β1水平较模型组显著降低(P0.05),海兔素高剂量组与低剂量组相比,肝脏病变改善程度更为明显(P0.05)。结论:海兔素对刀豆蛋白A诱导的化学性肝损伤具有一定保护作用,其机制可能与下调TNF-α、TGF-β1水平有关。     

Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring

Fetal nicotine exposure increased risk of developing cardiovascular disease later in life. The present study tested the hypothesis that perinatal nicotine-induced programming of heart ischemia-sensitive phenotype is mediated by enhanced reactive oxygen species (ROS) in offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in drinking water. Experiments were conducted in 8 month old age male offspring. Isolated hearts were perfused in a Langendorff preparation. Perinatal nicotine treatment significantly increased ischemia and reperfusion-induced left ventricular injury, and decreased post-ischemic recovery of left ventricular function and coronary flow rate. In addition, nicotine enhanced cardiac ROS production and significantly attenuated protein kinase C_ε (PKC_ε) protein abundance in the heart. Although nicotine had no effect on total cardiac glycogen synthase kinase-3β (GSK3β) protein expression, it significantly increased the phosphorylation of GSK3β at serine 9 residue in the heart. NAC inhibited nicotine-mediated increase in ROS production, recovered PKC_ε gene expression and abrogated increased phosphorylation of GSK3β. Of importance, NAC blocked perinatal nicotine-induced increase in ischemia and reperfusion injury in the heart. These findings provide novel evidence that increased oxidative stress plays a causal role in perinatal nicotine-induced developmental programming of ischemic sensitive phenotype in the heart, and suggest potential therapeutic targets of anti-oxidative stress in the treatment of ischemic heart disease.     

Possible Protective Effect of Kolaviron on CCl4-Induced Erythrocyte Damage in Rats

The possible protective effect of kolaviron on rat erythrocytes followingsimultaneous administration of kolaviron (100 mg/kg of body weight/day) withcarbon tetrachloride CCl₄ (1.195 g/kg of body weight/day) by separateintraperitoneal injections was investigated.Kolaviron, a biflavonoid fraction of the defatted alcoholic extract ofGarcinia kola seed, inhibits the accumulation of lipid peroxidationproducts in erythrocytes. A significant reduction (p>0.05) by about34% of lipid peroxidation products was observed in erythrocytes of ratstreated simultaneously with CCl₄ and kolaviron when compared to CCl4-treatedrats. Similarly, the significant increase (p>0.05) in membranecholesterol observed in CCl₄-treated rats was significantly decreased(p>0.05) in rats treated simultaneously with CCl4 andkolaviron. Therefore, there was no significant difference (p>0.05) incholesterol–phospholipid ratio (C/P) of rats treated simultaneouslywith CCl₄ and kolaviron, and the controls. Thus, kolaviron normalizes theCCl₄-induced change in erythrocyte membrane composition.In addition, kolaviron antagonizes the effect of CCl₄ on the activity ofthe membrane bound enzyme, Ca²⁺-ATPase. These results suggest thatkolaviron protects erythrocyte membranes from free radical attack, on bothlipids and proteins.     

稀土元素铈对花生幼苗生长与抗氧化保护酶系统的影响

采用溶液培养方法,研究不同浓度硝酸铈对花生(Arachis hypogaea)幼苗生长、开花数目及抗氧化酶过氧化物酶(POD)、超氧化物歧化酶(SOD)活性与丙二醛(MDA)含量的影响。结果表明,与对照相比,铈浓度低于20.0 mg·L–1能促进花生幼苗生长及开花,其中以10.0 mg·L–1铈的效果最为明显,其生物量和开花数分别约为对照的1.3倍和2.8倍;但高于20.0 mg·L–1则抑制花生幼苗生长,降低花朵数目;同时,低于20.0 mg/L铈可抑制花生幼苗过氧化物酶(POD)活性和降低其丙二醛(MDA)含量,其中以10.0 mg·L–1铈的抑制效果最明显,其POD活性和MDA含量约为对照的47.51%和20.76%;而低于20.0 mg·L–1铈能提高花生幼苗的超氧化物歧化酶(SOD)活性,其中以5.0 mg·L–1铈的促进效果最明显,其SOD活性约为对照的2.0倍。     

山楂果肉原花青素的体外抗氧化活性和对DNA损伤的保护作用

研究了化学发光法测定山楂果肉原花青素(procyanidins of Hawthorn Sarcocarp 简称HSPC)的体外抗氧化活性及其对DNA损伤的保护作用.运用邻苯三酚-鲁米诺化学发光体系测定了HSPC对超氧阴离子的清除作用,硫酸铜-邻菲啰啉-抗坏血酸-双氧水体系测定了HSPC对羟基自由基的清除作用,双氧水-鲁米诺体系测定了HSPC对体外双氧水的清除作用,采用硫酸铜-邻菲啰啉-抗坏血酸-双氧水-脱氧核糖核酸测定了HSPC对体外DNA损伤的保护作用.结果表明:当HSPC浓度为1 mg/mL时,对超氧阴离子抑制率达87.7%,其半数抑制率浓度IC50值为130.8 μg/mL;100 μg/mL时对羟基自由基抑制率达91.7%,IC50值为61.73 μg/mL;8 μg/mL时对双氧水抑制率达91.6%,IC50值为0.19 μg/mL;40 μg/mL时对体外DNA损伤抑制率达80.7%,IC50值为22.16 μg/mL.表明HSPC具有很好的体外清除活性氧和保护DNA损伤的活性.     

洛伐他汀联用格列本脲可改善高糖诱导损伤的HUVEC 功能

目的:探讨洛伐他汀与格列本脲联合用药对高糖诱导损伤的人脐静脉血管内皮细胞(HUVEC)的功能的影响及其机制。方法:以体外培养至第三代的HUVEC为研究对象,分四为:1空白对照组;2高糖组(33 mmol/L);3高糖组(33 mmol/L)+洛伐他汀(2μmol/L)组;4高糖组(33 mmol/L)+洛伐他汀(2μmol/L)+格列本脲(0.2μmol/L)组。用transwell小室法检测HUVEC的迁移功能,用细胞流式仪检测HUVEC内氧自由基(O~(2-))以及一氧化氮(NO)的表达水平。结果:与对照组相比,高糖组HUVEC迁移功能明显受损(P0.01);洛伐他汀单独用药组及其与格列本脲的联合用药组均能改善高糖损伤的HUVEC的迁移功能(均为P0.01)。流式结果显示,与对照组相比,高糖组HUVEC内O~(2-)水平明显增加而NO表达水平明显降低(均为P0.01);两组给药组HUVEC内O~(2-)水平及NO表达水平相对于高糖组均有明显改善(均为P0.01)。结论:洛伐他汀单独用药及其与格列本脲的联合用药均能改善高糖损伤的HUVEC的迁移功能,可能与改善细胞内氧化应激水平有关。     

Protective Effect of Agaricus blazei Polysaccharide Against Cadmium-Induced Damage on the Testis of Chicken

Biological Trace Element Research - Cadmium (Cd) exposure can cause reproductive toxicity through oxidative stress and inflammatory response. A polysaccharide extract of the edible mushroom...     

丙酮酸对细胞寒冷应激损伤的保护作用研究

目的:细胞冻存、移植器官保存过程中,机体细胞会产生细胞寒冷应激过程,导致细胞产生损伤作用,而其作用机制尚不清楚,本研究通过观察4℃冷暴露对HEK293细胞增殖活性及凋亡的影响,分析线粒体分裂蛋白Drp1在此过程中的表达变化,阐明Drp1在细胞寒冷应激中作用及其机制.方法:采用MTT法观察4℃环境暴露对HEK293细胞损伤的影响,流式细胞术检测细胞凋亡;Western blot方法检测蛋白Drp1、Bcl2表达水平变化,提取线粒体观察线粒体中Drp1表达水平.结果:4℃冷暴露抑制HEK293细胞增殖(P＜0.05),Drp1线粒体表达水平增高,并向线粒体转位;丙酮酸可以逆转4℃冷暴露对细胞增值抑制,抑制Drp1线粒体表达水平增高,并向线粒体转位,增加细胞中Bcl2表达水平.结论:研究发现细胞寒冷应激可以使细胞凋亡,细胞增殖出现显著抑制,而寒冷应激引起细胞Drp1的线粒体转位,丙酮酸干预后可以对细胞起到保护作用,研究发现丙酮酸可以逆转Drp1的线粒体转位过程,增加Bcl2表达水平,可能是其产生保护作用的机制之一.     

薄荷和罗勒提取物体外抗氧化及保肝活性研究

采用国际常用的ABTS和DPPH方法评价唇形科植物薄荷(Mentha haplocalyx) 和罗勒(Ocimum basilicum)水提物和乙醇提取物体外抗氧化活性,选用HepG2细胞,通过乙醇诱导损伤,构建体外酒精性肝损伤细胞模型,以细胞存活率评价薄荷和罗勒提取物的保肝效果。结果表明,DPPH自由基清除能力大小依次为薄荷醇提物、薄荷水提物、罗勒醇提物、罗勒水提物,半效应浓度(EC₅₀)分别为70.42 μg·mL^-1、75.77 μg·mL^-1、354.87 μg·mL^-1、451.53 μg·mL^-1。ABTS自由基清除能力大小依次为薄荷醇提物、罗勒醇提物、薄荷水提物、罗勒水提物,EC50值分别为9.04 μg·mL^-1、18.03 μg·mL^-1、22.18 μg·mL^-1、36.88 μg·mL^-1。薄荷提取物的抗氧化能力整体优于罗勒提取物,醇提物抗氧化能力优于水提物。酒精性肝损伤细胞活性检测表明,5、10、20、50 μg·mL^-1薄荷水提物、薄荷醇提物和罗勒水提物能剂量依赖性地提高乙醇诱导损伤的细胞存活率,具有一定的保肝活性。     

野菊水提物和醇提物抗氧化及保肝活性研究

采用ABTS和DPPH方法评价野菊Chrysanthemum indicum水提物和醇提物的抗氧化活性;选用HepG2细胞,通过乙醇诱导损伤,检测野菊水提物和醇提物处理后细胞存活率评价其保肝效果。结果表明,野菊醇提物抗氧化能力优于水提物,其中,野菊醇提物对ABTS自由基清除作用较好。酒精性肝损伤细胞活性测定显示,5、10、20μg·mL^-1的野菊水提物和醇提物处理组较乙醇损伤组(eth)细胞的存活率显著上升,总体呈现剂量依赖性,其中野菊醇提物保肝效果更优。