大鼠IL-10基因真核表达质粒的构建及其在BRL细胞中的表达

目的:构建大鼠IL-10基因的真核表达载体,观察其在大鼠肝细胞系BRL中的表达,比较有无受体介导的脂质体的转染效率.方法:抽提外周血单个核细胞的总RNA,通过RT-巢式PCR方法获得大鼠IL-10的全长编码序列,定向克隆到真核表达载体pcDNA3.0,并进行限制性内切酶酶切及测序鉴定.将重组质粒分别通过脂质体TransfastTM与去唾液酸糖蛋白受体介导的脂质体PEIjet-gal转入大鼠肝细胞系BRL,通过RT-PCR方法检测IL-10 mRNA的表达,比较二者的转染效率,用ELISA法检测后者分泌型IL-10的表达.结果:经酶切及测序鉴定证实,重组质粒插入片段与大鼠IL-10的全长编码序列完全相符.发现受体介导的脂质体PEIjet-gal转染效率明显高于非受体介导的脂质体TransfastTM .通过受体介导的脂质体转染,BRL细胞获得高水平的IL-10表达.结论:成功地构建pcDNA3.0-IL-10重组质粒.受体介导的脂质体对肝细胞有较高的转染活性,可能成为IL-10基因治疗肝纤维化的有效转染载体.     

不同载体转基因效率及AAV2介导bFGF基因在肌腱中表达的研究

目的:比较腺病毒、腺相关病毒和脂质体-质粒三种载体在肌腱中的基因转染效率并观测腺相关病毒载体介导bFGF基因在肌腱愈合过程中表达.方法:用微量注射器将携带增强绿色荧光蛋白报告基因的三种载体注射入正常肌腱中,用荧光显微镜观测术后不同时间点肌腱内EGFP的表达.将AAV2-bFGF病毒颗粒注入损伤肌腱,使用免疫组化染色观测bFGF在肌腱内表达.结果三种不同的载体转染肌腱3天后有EGFP表达、7天最明显、14天时下降;21天时少有表达.在同期的时间点,注射腺病毒、腺相关病毒组肌腱内EGFP表达明显强于质粒载体,而腺病毒、腺相关病毒两组之间无较大区别.免疫组化显示注射AAV2-bFGF后的第2、3和4周的肌腱表达很强的bFGF.结论:腺病毒、腺相关病毒载体的基因转染效率高于脂质体-质粒载体,AAV2携带的外源性bFGF基因在肌腱细胞内较强表达,提示我们将来在体内转基因到肌腱的研究中能够选择腺病毒和腺相关病毒载体作为运载基因的工具.     

真核过表达载体共转染3个胰岛发育关键基因在小鼠胎肝细胞内的表达*

背景：大量文献表明,向肝脏细胞引入一个多个胰岛发育的关键因子(如Pdx1、MafA及Ngn3)可以使肝细胞向胰岛细胞的方向进行转化。 目的：构建以pcDNA3.1(+)为骨架的质粒载体并共同转染胰十二指肠同源框蛋白(Pdx1)、神经源素3(Ngn3)及V型肌腱膜纤维肉瘤癌基因同源基因A(MafA)至小鼠胎肝细胞并检测其表达情况。 方法：以基因组或小鼠胰腺cDNA为模板扩增Pdx1、MafA及Ngn3三个目的基因,应用分子生物学技术,将3个目的片段克隆至真核表达载体pcDNA3.1(+)的多克隆位点中,构建小鼠系列真核过表达载体pcDNA3.1(+)-MafA ORF,pcDNA3.1(+)-Pdx-1 ORF,pcDNA3.1(+)-Ngn3 ORF通过Lipofectamine2000介导的脂质体转染小鼠胎肝细胞系BNL CL.2,用反转录PCR以及间接免疫荧光法检测3个目的基因的表达情况。 结果与结论：目的基因克隆正确,反转录PCR,间接免疫荧光法证实了脂质体转染后小鼠胎肝细胞中有Pdx1、Ngn3以及MafA的表达。结果表明,真核过表达载体pcDNA3.1(+)-MafA ORF,pcDNA3.1(+)-Pdx-1 ORF,pcDNA3.1(+)-Ngn3 ORF可成功构建,并能够将Pdx1、Ngn3以及MafA三个基因转至小鼠胎肝细胞进行表达。关键词：胰十二指肠同源框蛋白;神经源素3;V型肌腱膜纤维肉瘤癌基因同源基因A;脂质体转染;BNL CL.2细胞株;胰岛细胞;基因表达 doi:10.3969/j.issn.1673-8225.2012.18.018     

人甘露糖结合凝集素在小鼠肝脏细胞内表达

目的：在小鼠肝脏组织中表达人甘露糖结合凝集素（mannose-binding lectin，MBL）。方法：采用PCR方法从pGEMT-MBL质粒中扩增人MBLcDNA序列，克隆人pUC19载体中，限制性酶切鉴定及测序正确后，将MBLcDNA克隆人真核表达载体pcDNA3质粒中，构建成pcDNA3-MBL质粒，经尾静脉大容量快速注射pcDNA3-MBL质粒20μg，8h后处死小鼠，Western Blot方法检测小鼠肝脏组织和血清中人MBL，免疫组织化学方法检测小鼠肝脏组织中人MBL的表达情况。结果：成功扩增出人MBLcDNA序列并构建克隆载体pUC19-MBL，测序结果正确，成功构建pcDNA3-MBL真核表达载体。小鼠尾静脉注射pcDNA3-MBL质粒后8h，免疫组化检测证实肝细胞中有人MBL表达，Western blot方法检测发现血清和肝脏组织中出现人MBL蛋白。结论：真核表达载体pcDNA3-MBL裸质粒DNA静脉注射可以在小鼠肝脏中大量表达人MBL，并分泌人血，为临床纠正先天性低MBL患者的易感染状态提供了新的思路。     

腺病毒相关病毒增强型mIL-10质粒的构建及表达

构建腺病毒相关病毒增强型mIL 10质粒 ,并在心肌细胞内进行表达。利用分子克隆技术 ,将腺病毒相关病毒 (AAV )中的末端重复序列 (ITR )插在pORF5 mIL 10质粒启动子的上游 ,构建pORF AAV mIL 10质粒。在阳离子脂质体Lipofectin介导下 ,pORF5 mIL 10和pORF AAV mIL 10分别转染次代培养心肌细胞 ,TRIzol一步法提取总RNA ,RT PCR检测mIL 10的mRNA ;ELISA检测培养细胞上清中mIL 10的表达。结果是用双酶切证实成功构建质粒 ,分别在转染 2 4h、 4 8h、 72h、 96h、 12 0h后 ,用RT PCR在心肌细胞中检测到相应的目的条带 ,ELISA检测各组mIL 10的表达量。证实在阳离子脂质体Lipo fectin介导下 ,pORF AAV mIL 10能在一定时间内稳定的增加mIL 10在心肌细胞内的表达。     

脂质体介导转染N2a细胞的优化方法

背景:阳离子脂质体介导的细胞转染具有结果可靠、可重复性强的特点,但面临一个共同的缺点,就是转染效率常较低。目的:探讨阳离子脂质体转染N2a细胞(小鼠神经胶质瘤细胞)的优化方法。方法:采用24孔培养板,1.5μL阳离子脂质体Lipofectamine?LTX介导,通过贴壁法和悬浮法,将500 ng带有绿色荧光蛋白(GFP)基因的重组质粒pcDNA3-GFP转入N2a细胞,倒置荧光显微镜观察细胞内绿色荧光蛋白表达情况,并比较二者转染效率。采用悬浮转染法,将500 ng质粒DNA分别用1.0,1.5,2.0,2.5μL Lipofectamine?LTX进行转染,探讨最适脂质体和DNA比例。结果与结论:1.5μL脂质体/500 ng DNA,悬浮法转染效率显著高于贴壁法转染效率(P0.01);1.0,1.5,2.0,2.5μL Lipofectamine?LTX对500 ng质粒DNA的转染效率分别为(76.60±3.85)%,(80.00±4.17)%,(88.00±5.89)%,(54.96±4.23)%,提示脂质体2.0μL与质粒DNA 500 ng的转染效率最高。     

阳离子脂质体介导的基因转移机制

背景：与病毒载体相比,许多天然与合成的阳离子类脂以脂质体的形式用于基因转移,具有无免疫原性、易生产、质粒免受核酸酶降解和无致瘤性等优点,并且作为病毒载体的有效替代物,阳离子脂质体能用于细胞的体内和体外转染。 目的：介绍阳离子脂质体介导的基因转移机制研究进展。 方法：由第一作者用计算机检索中国期刊全文数据库(CNKI：1987/2010)和PubMed (1987/2010)数据库,检索词分别为“基因治疗、阳离子脂质体、基因转移、机制”和“gene therapy, cationic liposome, gene transfer, mechanism”,语言分别设定为中文和英文。从阳离子脂质体基因转染和基因转移机制进行总结,综述了阳离子脂质体介导的基因转移机制。 结果与结论：共检索到108篇,按纳入和排除标准对文献进行筛选,共纳入20篇文章。综述了阳离子脂质体介导的基因转移机制,包括阳离子脂质体/DNA复合物的形成、细胞吸收、内含体释放和复合物解体以及细胞核摄入等方面的研究内容。结果提示,对类脂构效关系和基因转移机制的研究,是提高阳离子脂质体转染效率和优化基因治疗的关键。     

脂质体介导弓形虫SAG1与SAG3复合基因诱导小鼠免疫应答研究

目的评价弓形虫SAG1与SAG3基因真核表达质粒DNA免疫小鼠的免疫应答效果。方法以PCR方法扩增出SAG1与SAG3目的基因片段,并插入载体pEGFP-N3以构建重组质粒pE- SAG1／SAG3,瞬时转染细胞Cos-7。质粒pESAG1／SAG3以10μg剂量,脂质体介导肌肉注射BALB／c小鼠,免疫3次,最后一次免疫后4周,观察体液和细胞免疫。RT-PCR方法检测注射部位目的基因的转录;斑点杂交方法检测目的基因是否与小鼠染色体基因组整合。结果质粒pESAG1／SAG3转染细胞后观察到绿色荧光;Western blot显示pESAG1/SAG3表达识别条带在相对分子质量(Mr)66．2×103附近。小鼠免疫后,血清产生抗弓形虫速殖子抗体,诱导IFN-γ及IL-2水平高于对照组。RT-PCR显示首次免疫15 d后,目的基因在肌肉组织中仍有转录,斑点杂交显示目的基因未与小鼠的基因组发生整合,混合质粒注射的小鼠抗弓形虫感染的存活时间延长。结论脂质体介导弓形虫SAG1与SAG3复合编码基因质粒接种小鼠能明显诱导体液和细胞免疫应答。     

肝脏靶向表达趋化因子CXCL10 抑制ConA 诱导的肝脏损伤

目的:本研究探索趋化因子CXCL10 在免疫介导的肝脏损伤方面的作用及其作用机制。方法:尾静脉高压注 射CXCL10 表达载体72 h 后检测肝脏中CXCL10 的表达水平;再尾静脉注射刀豆蛋白(Concanavalin A,ConA)诱导免疫介导的 肝脏损伤;检测并比较CXCL10 表达组和对照组的谷丙转氨酶(Alanine aminotransferase,ALT)水平、组织损伤水平、,IFN-γ水 平、TNF-α水平及调节性T 细胞比例和数量的差异。结果:CXCL10 表达载体注射72 h 后,肝脏中CXCL10 的表达水平显著升 高;CXCL10 表达质粒预处理可以有效减轻ConA 诱导的肝脏损伤,CXCL10 表达组小鼠血清中的ALT 水平显著低于对照组, CXCL10 表达组小鼠血清中,IFN-γ和TNF-α的水平明显低于对照组,CXCL10 表达组小鼠肝脏中调节性T 细胞比例和数量高 于对照组。结论:趋化因子CXCL10 表达载体预处理可减少炎性细胞因子并减轻ConA 诱导的肝脏损伤,对治疗免疫介导的肝 炎具有重要意义。     

乙型肝炎病毒多表位抗原基因真核表达载体的构建及其在哺乳动物细胞中的表达

将自行设计、合成的乙型肝炎病毒多表位抗原基因BPT ,克隆入真核表达载体pCDNA3 1,构建重组质粒pCDNA3 1/BPT。后者经脂质体法转染小鼠BALB/c 3T3细胞 ,G4 18加压筛选出阳性转染细胞 ,并用间接免疫荧光法鉴定其在小鼠BALB/c 3T3细胞的表达。该重组质粒经胫骨前肌注射小鼠 ,10 0 μg/次每只小鼠 ,间隔 2周加强一次 ,共 3次。免疫诱发了特异性抗体和淋巴细胞增殖反应 ,并用PCR法在小鼠的心脏、肝脏及肺组织中检测到pCDNA3 1/BPT ,这为研究HBV多表达抗原的核酸疫苗提供了初步的资料     

A nitric oxide-releasing reagent, S-nitroso-N-acetylpenicillamine, enhances the expression of superoxide dismutases mRNA in the murine macrophage cell line RAW264-7.

Murine interferon-gamma (IFN-gamma) stimulates the murine macrophage tumour cell line RAW264-7 to produce nitric oxide (NO). IFN-gamma induces expression of inducible NO synthase (iNOS), manganese superoxide dismutase (Mn-SOD) and copper zinc SOD (CuZn-SOD) in these cells. To investigate the mechanism of induction of SOD expression, we added S-nitroso-N-acetyl penicillamine (SNAP) to RAW264-7 cells. SNAP enhanced the expression of Mn-SOD and CuZn-SOD. These results suggest that when producing NO, RAW264-7 cells express SOD that might protect them from NO toxicity.     

Superoxide dismutases in Eimeria tenella.

Unsporulated oocysts of Eimeria tenella have high superoxide dismutase (SOD: superoxide:superoxide oxidoreductase, EC 1.15.1.1.) activity and contain several electrophoretically distinct forms of the enzyme, including two forms of Cu/Zn-containing SOD, two forms of Fe-SOD and two forms of Mn-SOD. SOD activity remains high during 12 h of sporulation but diminishes slowly during prolonged sporulation. Oocysts sporulated for 48 h have low levels of superoxide dismutase and contain only one form of the enzyme (Mn-SOD), which was also found in sporozoites. In vitro, sporozoites are oxidant-sensitive and die within minutes of superoxide radical (O2-) generation but SOD/catalase and mannitol protect sporozoites against oxidative damage. These data suggest that E. tenella sporulated oocysts and sporozoites lack soluble cytoplasmic SOD and that this deficiency may contribute to the oxidant sensitivity of the parasite.     

当归多糖治疗小鼠乙醇性肝损伤中丙二醛、超氧化物歧化酶及谷胱甘肽过氧化物酶的变化及意义

目的:探讨当归多糖治疗小鼠乙醇性肝损伤中丙二醛(MDA)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSHPx)的变化及意义。方法:通过一次性高浓度乙醇灌胃建立小鼠乙醇性肝损伤模型,之后连续腹腔注射当归多糖6 d,血清生化检测MDA、SOD及GSH-Px,光镜观察肝形态结构变化。结果:小鼠乙醇性肝损伤后,血清MDA显著增高,SOD及GSH-Px显著下降,同时肝组织结构呈弥漫性脂肪变性损伤。用当归多糖治疗后,伴随肝组织结构的修复,血清MDA显著下降,SOD及GSH-Px增高。结论:当归多糖可通过阻断膜脂质过氧化起到保护肝细胞的作用,血清MDA、SOD及GSHPx水平的变化对判断肝的损害程度、病情发展、评估预后有一定的意义。     

SOD2启动子的克隆及转录活性的检测

目的： 克隆小鼠锰超氧化物歧化酶基因(MnSOD, SOD2) 5非编码区启动子序列，通过报告基因技术检测在静息或脂多糖（LPS）、亚砷酸钠(NaAsO2)等刺激下该段启动子的转录活性。方法: 提取小鼠肝组织基因组DNA，PCR扩增小鼠SOD2启动子序列(-1 554～+48)；采用基因重组技术构建由SOD2启动子驱动的红色荧光蛋白报告基因载体，将该载体瞬时转染小鼠胚胎成纤维细胞(MEF)，荧光显微镜下观察静息或NaAsO2、LPS、佛波酯(PMA)刺激下红色荧光蛋白表达。结果: 正确扩增出小鼠SOD2启动子(-1 554～+48)片段；成功构建其红色荧光蛋白报告基因载体，证实该质粒转染MEF细胞后静息状态下仅可见少量而微弱的红色荧光，经NaAsO2、LPS、PMA刺激后，红色荧光强度和亮度明显增加。结论: 小鼠SOD2启动子(-1 554～+48)在静息状态下即具有转录活性，炎性、氧化应激刺激后SOD2表达增强；该启动子的成功克隆和其报告基因载体的构建，为研究SOD2的基因表达调控机制提供了重要基础和工具。     

NF-κB参与低氧预适应对自体原位肝移植大鼠JNK通路的影响

背景：在肝脏缺血再灌注损伤中,NF-κB与JNK通路的串扰方式决定了细胞的死亡或存活。而将低氧预适应用于肝移植过程所导致的细胞凋亡现象,尚未见有报道。 目的：探讨低氧预适应后NF-κB的表达对移植肝JNK通路的影响及保护作用。 方法：采用经门静脉灌注法建立大鼠自体原位肝移植模型,SD大鼠随机分为正常对照组：不接受任何处理;自体移植组：行自体原位肝移植;低氧预适应组：移植前体积分数8%氮氧混合气体的低氧预处理90 min,然后行自体原位肝移植。分别于移植后 1,6,24 h处死大鼠取肝脏标本检测肝组织丙二醛、超氧化物歧化酶水平,免疫组化方法测定大鼠肝组织p-JNK蛋白,RT-PCR检测肝脏 NF-κB mRNA含量,透射电子显微镜下观察肝细胞的超微结构变化。 结果与结论：与对照组比较,两移植组肝组织丙二醛水平升高,超氧化物歧化酶水平降低(P < 0.05);与自体移植组比较,低氧预适应组丙二醛水平显著降低、超氧化物歧化酶水平显著升高(P < 0.05)。与正常对照组比较,两移植组各时相p-JNK蛋白的表达、NF-κB mRNA的转录水平显著升高 (P <0.05);与自体移植组比较,低氧预适应组NF-κB mRNA转录水平显著增高(P < 0.05),p-JNK蛋白的表达明显降低(P < 0.05)。透射电镜下自体移植组肝细胞出现典型的凋亡征象,而低氧预适应组肝细胞无明显凋亡形态。提示,肝移植大鼠低氧预适应后可能通过上调NF-κB的表达,减少活性氧释放,抑制JNK通路的持续激活,从而抑制肝细胞凋亡,减轻肝脏缺血再灌注。     

Age-related changes in manganese superoxide dismutase activity in the cerebral cortex of senescence-accelerated prone and resistant mouse

In this paper, we showed that the oxidative stress in brain of senescence-accelerated prone mouse 8 (SAMP8) at earlier stages was increased compared with that of senescence-accelerated resistant mouse 1 (SAMR1) irrespective of the breeding conditions. Furthermore, we found that manganese superoxide dismutase (Mn-SOD) activity in the cerebral cortex of 10-week-old SAMP8 was decreased by about 50% compared with that in age-matched SAMR1. These results indicate that the decrease of Mn-SOD activity may be involved in the increased oxidative stress in the brain of SAMP8 at younger stages. However, there was no difference in the expression of this protein between the two strains at 10 weeks of age, suggesting that Mn-SOD protein in SAMP8 was post-translationally modified to reduce its enzymatic activity.     

Different mechanisms for the induction of copper-zinc superoxide dismutase and manganese superoxide dismutase by progesterone in human endometrial stromal cells

BACKGROUND: The present study was undertaken to investigate the cAMP-dependent regulation of copper-zinc superoxide dismutase (Cu,Zn-SOD) and manganese SOD (Mn-SOD) by ovarian steroids in human endometrial stromal cells (ESC). METHODS and RESULTS: To examine the effect of cAMP on SOD expression, ESC were incubated with dibutyryl-cAMP (db-cAMP, 0.5 mmol/l), forskolin (25 micromol/l), or estradiol (E(2), 10(-8) mol/l) + medroxyprogesterone acetate (MPA, 10(-6) mol/l), for 18 days. E(2) + MPA significantly increased Cu,Zn-SOD activity and mRNA concentrations, whereas db-cAMP and forskolin had no effect. On the other hand, Mn-SOD activity and mRNA concentration were significantly increased by all of these treatments. Insulin-like growth factor-binding protein-1, a marker of decidualization, was clearly induced by db-cAMP, forskolin or E(2) + MPA, accompanied by morphological changes characteristic of decidualization. To study whether the increase in Mn-SOD by db-cAMP or E(2) + MPA was mediated by cAMP-dependent protein kinase A (PKA), ESC were incubated with protein kinase inhibitor (PKI) (10 microg/ml), an inhibitor of PKA, in the presence of db-cAMP or E(2) + MPA. The increase in Mn-SOD activity following db-cAMP or E(2) + MPA was completely inhibited by PKI. CONCLUSIONS: In the process of decidualization, E(2) + MPA increases Mn-SOD expression via a cAMP-dependent pathway. Cu,Zn-SOD is also up-regulated by E(2) + MPA, but via a different pathway from that involving cAMP.     

Protective effects of Cu/Zn-SOD and Mn-SOD on UVC radiation-induced damage in NIH/3T3 cells and murine skin

Superoxide dismutase (SOD) is an antioxidant enzyme with multiple metal cofactors that can specifically clear reactive oxygen species (ROS), which plays an important role in a variety of ultraviolet-induced lesions. Therefore, SOD has the anti-ultraviolet radiation effect. The objective of this study was to compare the differences in the anti-ultraviolet radiation effect of SOD with distinct metal cofactors: Cu/Zn-SOD and Mn-SOD. SOD was first purified using hydrophobic interaction chromatography and ion-exchange chromatography. Second, the Methylthiazolyldiphenyl-tetrazolium bromide method and cell senescence kits were used to study the protective effect of SOD on ultraviolet-induced cell damage. Finally, the protective effect of SOD on ultraviolet -induced skin damage was histopathologically evaluated, and the expression levels of malondialdehyde (MDA) and matrix metalloproteinases (MMPs) in tissues were detected. The results showed that Cu/Zn-SOD was superior to Mn-SOD in promoting cell proliferation, alleviating cell damage, protecting skin structure, and regulating the expression levels of MDA and MMPs, and it has no side effects. In conclusion, Cu/Zn-SOD had a better anti-ultraviolet radiation effect than Mn-SOD, and it can be used in anti-aging and anti-ultraviolet skin-care products.     

Differential mucosal expression of three superoxide dismutase isoforms in inflammatory bowel disease

Mucosal tissue damage and dysfunction in chronic inflammatory bowel disease (IBD) are partly caused by an enduring exposure to excessive amounts of reactive oxygen metabolites (ROMs). Although the three human isoforms of superoxide dismutase (SOD), copper/zinc (Cu/Zn)-SOD, manganese (Mn)-SOD, and extracellular (EC)-SOD, form the primary endogenous defence against ROMs, their expression levels and cellular localization in IBD mucosa are largely unknown. The present study used enzyme-linked immunosorbent assays (ELISAs), spectrophotometric activity assays, and immunohistochemistry to evaluate the protein concentration, enzymatic activity, and distribution of Cu/Zn-, Mn-, and EC-SOD in paired inflamed and non-inflamed mucosal resection specimens of patients with Crohn's disease (CD) or ulcerative colitis (UC) and compared these with the levels obtained in normal control mucosa. Gut mucosal SOD isoform expression was found to be differentially affected in IBD patients, without major differences between CD and UC. A marked step-wise increase in Mn-SOD protein levels was observed in non-inflamed and inflamed IBD mucosae, whereas the Cu/Zn-SOD content decreased with inflammation. EC-SOD was only found in low amounts, which tended to be decreased in IBD patients. Immunohistochemical evaluation confirmed these observations. Mn-SOD and Cu/Zn-SOD were both predominantly expressed in intestinal epithelial cells and the percentage of epithelial cells positive for Mn-SOD was considerably increased in IBD, whereas epithelial Cu/Zn-SOD expression was much less affected. Within the lamina propria, SOD expression was much lower. Cu/Zn-SOD and Mn-SOD were prominently present in neutrophils and macrophages, and EC-SOD was mainly localized in small vessels, stromal cells, and neutrophils. The percentage of lamina propria cells positive for Cu/Zn-, Mn-, or EC-SOD was not affected by inflammation. Enzyme activity measurements showed consistent results for Cu/Zn-SOD and EC-SOD, but the activity of Mn-SOD did not concordantly increase with the immunological assessments, which may indicate that a proportion of the Mn-SOD in IBD is present in an enzymatically inactive form. This study reveals remarkable changes in the expression levels of the three SOD isoforms in IBD, particularly in the epithelium. Disturbances in the carefully orchestrated mucosal antioxidant cascade may contribute to the induction and perpetuation of intestinal inflammation in IBD, and may have important implications for the development of antioxidant treatment of IBD patients.