缺氧环境下MSCs促进血管内皮细胞增殖和血管形成

目的 探讨成人骨髓间充质干细胞(bone marrow mesenchymal stem cells BMSCs)在体外缺氧环境下对人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)增殖和血管形成能力的影响及其可能机制.方法密度梯度离心法收集分离成人骨髓血MSCs并进行体外培养扩增,传代至4代进行实验,流式细胞仪鉴定MSCs表面标志.BMSCs缺氧培养0h(对照组)、12h、24h和48h后,RT-PCR检测SDF-1和VEGF基因表达,ELISA法检测细胞上清液中SDF-1和VEGF蛋白含量.HUVECs传代培养后分成三组进行实验:对照组、BMSCsCMN-HUVECs组,BMSCsCMH-HUVECs组,MTT检测三组细胞增殖能力,体外血管形成实验分析三组细胞在Matrigel上管腔样结构形成情况.结果 (1) BMSCs呈旋涡状长梭形即纤维母细胞样生长;(2) 人BMSCs阳性表达CD29、CD44和CD90,而CD34、CD45和CD106为阴性;(3) BMSCs缺氧培养后SDF-1和VEGF在mRNA和蛋白水平表达均较常氧培养显著增高(P均<0.05);(4) BMSCsCMH明显提高HUVECs增殖能力(P<0.05),显著增加HUVECs在Matrigel上形成管腔样结构的能力(P<0.05).结论 人BMSCs在缺氧环境下通过旁分泌SDF-1和VEGF提高血管内皮细胞增殖和管腔样结构形成能力,促进血管新生.     

中性粒细胞mGluRI的激活促进其与内皮细胞相互黏附

本文旨在探讨I组代谢型谷氨酸受体(group I metabotropic glutamate receptor,mGluRI)在中性粒细胞上的表达,以及该受体的激活对中性粒细胞与内皮细胞相互黏附的影响。取健康人新鲜静脉血,Ficoll-Hypaque密度梯度离心法分离中性粒细胞,免疫细胞化学法和real-time PCR法检测中性粒细胞mGluRI(包括mGluR1和mGluR5)的表达,分别应用不同浓度的mGluRI特异性激动剂S-3,5-二羟基苯甘氨酸(S-3,5-dihydroxy-phenylglycine,S-DHPG)处理中性粒细胞不同时间,通过比色法检测中性粒细胞和人正常脐静脉内皮细胞(human normal umbilical vein endothelial cells,HUVE-12)黏附率,采用流式细胞术测定中性粒细胞黏附分子CD11a表达的变化。结果证实中性粒细胞表达mGluRI(mGluR1/5);S-DHPG在1×10-8~1×10-6mol/L浓度范围内呈剂量依赖性地提高中性粒细胞与内皮细胞之间的黏附率(P0.05或P0.01);1×10-6mol/L S-DHPG单独作用于中性粒细胞0.5h,即可促进中性粒细胞黏附于内皮细胞(P0.01),但没有时间依赖性;1×10-6mol/L S-DHPG单独作用于中性粒细胞可促进CD11a表达(P0.01);mGluRI拮抗剂(RS)-α-甲基-4-羧基苯甘氨酸[(RS)-α-methyl-4-carboxyphenylglycine,(±)-MCPG](0.5mmol/L)可以显著阻断激动剂S-DHPG(1×10-6mol/L,1h)的促黏附效应(P0.01)。上述结果证实了中性粒细胞膜上mGluRI的激活可增强中性粒细胞表面黏附分子CD11a的表达,促进中性粒细胞与内皮细胞的黏附。     

补骨脂素对中波紫外线导致人皮肤HaCaT细胞光老化的保护作用

目的:研究补骨脂素对中波紫外线(UVB)导致人皮肤HaCaT细胞光老化的保护作用及其作用机制。方法:选择不同浓度的补骨脂素,MTT法筛选药物的浓度;使用中波紫外线(UVB)照射永生化的HaCaT细胞建立UVB光老化模型;使用三种不同浓度的补骨脂素处理光老化模型,MTT法检测细胞的增殖及氧化试剂盒检测细胞中氧化酶的活性。RT-PCR及Western Blot分别检测JNK和白介素-8(IL-8)mRNA及蛋白表达量。结果:与空白组相比,10~(-7)mol/L、10~(-6)mol/L、10~(-5)mol/L补骨脂素组对HaCaT具有无明显的增殖作用(P0.05);与模型组相比,10~(-7)mol/L、10~(-6)mol/L、10~(-5)mol/L补骨脂素组对HaCaT具有无明显的增殖作用(P0.05),但是10~(-7)mol/L、10~(-6)mol/L、10~(-5)mol/L补骨脂素组SOD、GSH、CAT活性升高(P0.01),细胞JNK、IL-8 mRNA表达量均降低(P0.01),细胞JNK、IL-8蛋白表达量均降低(P0.05或P0.01)。结论:补骨脂素能够显著的保护HaCaT细胞的光老化,其机制可能与增强抗氧化酶活性,及抑制JNK信号通路,减少炎症因子的分泌有关。     

睾酮对人血管内皮细胞产生NO、tPA和PAI-1的影响

目的:观察不同浓度睾酮对人血管内皮细胞生长、产生舒张因子及纤溶活性的影响.方法:体外培养人脐静脉内皮细胞(HUVEC),分为五个浓度睾酮组及单纯培养基对照组.做MTT实验观察睾酮对HUVEC生长的影响;还原酶法测定各组HUVEC释放NO量;ELISA法测定各组培养基中纤溶酶原激活物(tPA)及其抑制物(PAI-1)含量.结果:3×10-10mol/L-3×10-8mol/L睾酮组与对照组相比细胞生长良好,无明显差别;而大于生理剂量的两组(3×10-6～3×10-1mol/L)3 d后细胞生长明显受到抑制(P＜0.05).各浓度睾酮组产生NO量与对照组无明显区别.而3×10-10 mol/L～3×10-8 mol/L睾酮组tPA含量明显高于对照组(P＜0.01);大剂量组tPA产生明显减少(P＜0.01).所有实验组的PAI-1含量均明显降低.结论:生理及略低于生理剂量的睾酮对HUVEC生长及释放NO无不利影响,且增加纤溶活性.说明生理剂量睾酮对血管内皮功能、心血管系统有一定的保护作用,有利于防止动脉粥样硬化的发生、发展.     

云南昭通年青褐煤黄腐酸钠对血管新生作用的影响

研究云南昭通地区年青褐煤黄腐酸钠对体内外血管新生作用的影响。将不同浓度的黄腐酸钠作用于人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)体外模型和鸡胚绒毛尿囊膜(chick chorioallantoic membrane,CAM)体内模型,采用MTT和划痕法检测其对HUVECs增殖和迁移的影响,以ELISA试剂盒测定细胞上清液血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达,采集CAM图片用Image-Pro Plus6.0软件考察给药区域血管新生的情况。结果显示,与对照组比较,云南昭通年青褐煤黄腐酸钠在100、200、400μg/m L的浓度下对HUVECs的增殖有抑制作用(P0.05,P0.01),在100、200μg/m L浓度时对迁移有抑制作用并能下调血管内皮生长因子VEGF的表达(P0.01),在高浓度800、1200μg/m L下能抑制CAM血管的新生(P0.05)。研究结果表明,云南昭通地区年青褐煤黄腐酸钠具有良好的血管新生抑制作用,其机制可能与生长因子VEGF表达的下调有关。     

CGRP抑制AngⅡ诱导HUVECs的损伤及其ERK1/2信号通路

目的:探索降钙素基因相关肽(CGRP)对经血管紧张素Ⅱ (AngⅡ)损伤的人脐静脉内皮细胞(HUVECs)的保护作用且CGRP与细胞外信号调节激酶(ERK1/2)的关系.方法:不同浓度的CGRP、AngⅡ处理体外培养的HUVECs,噻唑蓝比色法检测HUVECs活力;流式细胞仪分析HUVECs凋亡率及其增殖指数;显微镜观察HUVECs的形态学变化;Western blot检测p-ERK1/2的表达.结果:AngⅡ (0.1-100 nmol/L)浓度依赖性降低HUVECs的活力,而CGRP (0.1-1000 nmol/L)浓度依赖性增加HUVECs的活力;HUVECs增殖指数PI值受AngⅡ、CGRP及PD98059(ERK1/2抑制剂)影响;AngⅡ孵育HUVECs在第10min时ERK1/2磷酸化水平可达到最大;CGRP能抑制AngⅡ诱导的HUVECs内ERK1/2磷酸化水平;CGRP8-37(CGRP受体拮抗剂)可部分减弱CGRP抑制ERK1/2磷酸化水平作用;PD98059(ERK1/2抑制剂)作用下,ERK1/2磷酸化水平显著降低,但是对细胞内总ERK1/2水平表达无明显影响.结论:CGRP可抑制AngⅡ对HUVECs的损伤作用,可能与CGRP抑制信号通路ERK1/2有关.     

芒果苷对高糖诱导下系膜细胞自噬的影响

本文旨在探讨芒果苷对高糖诱导系膜细胞增殖的抑制作用,并从自噬角度阐述可能的机制。采用CCK8法检测芒果苷对高糖诱导系膜细胞增殖的抑制作用,Western blot检测芒果苷给药24 h后LC3-II蛋白的表达,采用GFP-LC3绿色荧光视踪检测芒果苷对系膜细胞自噬体数量的影响。结果表明:与高糖组相比,芒果苷5×10~(-5)、1×10~(-5)、5×10~(-6)mol/L能明显改善系膜细胞增殖(P0.01)。与高糖组相比,芒果苷给药24 h后5×10~(-5)、1×10~(-5)mol/L组LC3-II蛋白的表达升高(P0.05)。芒果苷给药组(1×10~(-5)、2×10~(-5)、4×10~(-5)、8×10~(-5)mol/L)1 h、3 h GFP-LC3绿色点状荧光明显增多。提示芒果苷具有抑制高糖诱导下系膜细胞的增殖作用,其机制可能是通过提高系膜细胞自噬水平,从而维持细胞内环境的稳定。     

前列腺素E2对小鼠骨髓细胞增殖及DNA合成的影响

本文采用半固体单层琼脂培养和液体培养_3H-TdR掺入法观察PGE_2对小鼠骨髓CFU-GM增殖分化的影响,实验结果表明PGE_2可明显抑制CFU-GM增殖和分化,抑制率与PGE_2剂量呈负相关。其50％抑制率所对应的PGE_2剂量,琼脂培养法为4.8×10~(-8)mol/L, ~3H-TdR掺入法为3.5×10~(-8)mol/L,两种方法观察的结果相近。压片染色集落分类的结果还表明PGE_2对CFU-GM各类型集落形成均有明显的抑制作用。其中以CFU-M和CFU-GM抑制最为明显。1×10~(-8)—1.2×10~(-8)mol/L的PGE_2浓度就可抑制CFU-M和CFU-GM增殖50％,当PGE_2浓度增至7.3×10~(-8)mol/L时CFU-M增殖即被抑制90％,说明单核-巨噬系祖细胞对PGE_2是十分敏感的。PGE_2对粒系集落的抑制作用机理尚不清楚。     

抗氧化剂丹酚酸A对缺氧鼠肺内动脉ACh舒张反应的影响

应用微量生物测定法观察了丹酚酸A(salvinolic acid A,Sal.A)对慢性缺氧(5000m,10d)大鼠(200～300g)肺内动脉ACh舒张反应的影响,并对其机制进行了初步探讨。实验发现,慢性缺氧可明显减弱大鼠肺内动脉ACh(10~(-8)～10~(-4)mol/L)舒张反应(P<0.01～0.001),在浴槽内先加入Sal.A(10~(-4)mol/L),缺氧鼠肺内动脉ACh舒张反应明显增强(P<0.01),而在浴槽内同时加入血管内皮舒张因子(EDRF)灭活剂phenidon(5×10~(-5)mol/L),则Sal.A上述增强缺氧鼠肺内动脉ACh舒张反应的作用消失。此外,本实验还发现,在以黄嘌呤(X,10~(-4)mol/ L)-黄嘌呤氧化酶(XO,0.01U/ml)系统产生氧自由基损伤正常大鼠肺内动脉ACh舒张反应的基础上,Sal.A(10~(-4)mol/L)同样可明显减弱氧自由基对大鼠肺内动脉ACh舒张反应的损伤作用。结果表明,Sal.A可消除氧自由基对肺血管内皮细胞释放的EDRF的破坏作用而具有保护慢性缺氧鼠肺内动脉ACh舒张反应的作用。     

AGEs通过SDF-1/CXCR4轴信号通路对心肌微血管内皮细胞血管新生的影响及机制

目的:探讨AGEs通过刺激SDF-1/CXCR4轴信号系统对心肌微血管内皮细胞的增值、迁移、管样结果形成的影响以及AMD3100对其的干预作用.方法:用不同浓度的AMD3100作用于浓度为200mg/L的AGEs共孵育的CMECs24h,用MTT法检测细胞活力及增殖能力,并选择合适的干扰浓度(抑制效果居中).随机选取加入AGEs200ml/L的CMECs,加入合适浓度的AMD3100,分别作用24、48、72h,采用MTT法测定AGEs处理前后细胞增值率的变化,并检测AMD3100对增值率的影响;毛细血管管腔样结构形成实验检测对CMECs血管新生的影响和AMD3100对其阻断作用的影响.结果:心肌微血管内皮细胞增殖能力和迁移能力在24h、48h、72h有显著增强;并促进了心肌微血管内皮细胞管样形成(vs P＜0.05);CXCR4受体阻断剂AMD3100作用于细胞后,可以显著阻断AGEs对心肌微血管内皮细胞增殖能力和迁移能力和管腔形成(vs P＜0.05)的影响.结论:AGEs在早期显著增强了心肌微血管内皮细胞的增殖、迁移和管样结构形成的能力,其作用机制可能与SDF-1/CXCR4轴信号通路有关.     

雌激素对A549细胞系EMT过程的影响

目的:探讨雌激素对A549细胞系EMT标志物表达量的影响。方法:用不同浓度的雌激素刺激A549细胞系,并用q-RT-PCR和Western-blot实验检测各组细胞中EMT标志物表达量的变化,用Transwell实验检测不同浓度雌激素对细胞迁移能力的影响,计算各组间有无统计学差异。结果:当雌激素浓度为1×10-9 mol/L、1×10-8 mol/L、1×10-7 mol/L时,Vimentin的m RNA表达量分别为:2.14±0.55、4.72±0.63、2.21±0.47,显著高于空白对照组,组间有统计学差异,E-cadherin的m RNA表达量分别为:0.64±0.15、0.46±0.11、0.59±0.13,显著低于空白对照组,组间有统计学差异,蛋白表达量也有同样趋势;细胞迁移数分别为58.63±7.33、80.12±9.32、61.89±8.22,组间有统计学差异。当雌激素浓度为1×10-8 mol/L时,Vimentin的表达量最高,E-cadherin的表达量最低,细胞迁移数最高。结论:适宜浓度雌激素可以促进Vimentin的表达,抑制E-cadherin的表达,提高细胞迁移能力,当雌激素浓度为1×10-8 mol/L时,促进Vimentin表达、抑制E-cadherin表达和促进细胞迁移的作用最显著。由此认为,雌激素对A549细胞系发生EMT过程有促进作用。     

Hydrogen sulfide delays nicotinamide-induced premature senescence via upregulation of SIRT1 in human umbilical vein endothelial cells

The present study was designed to investigate the effect of hydrogen sulfide on cellular senescence of human umbilical vascular endothelial cells (HUVECs CC-2517) and its underlying mechanism. The premature senescence-like phenotype HUVECs (the fourth passage) was induced by treatment with nicotinamide (NAM, an inhibitor of SIRT1, 5 mmol/L, 12 h). Cells were cultured with sodium hydrosulfide (NaHS, 12.5, 25, 50 and 100 μmol/L) for 48 h in premature senescence-like phenotype HUVECs. The fourth passage of HUVECs was considered as young group. Senescence-associated (SA)-β-galactosidase activities were detected to evaluate cell senescence, and the expression of SA heterochromatin foci (SAHF) was visualized by DAPI DNA staining. The mRNA and protein levels of SIRT1 were detected using RT-PCR and western blotting analysis, respectively. The results showed that β-galactosidase positive cells and the formation of SAHF were markedly increased after treatment with NAM (5 mmol/L) for 12 h. We also found that NaHS (12.5 μmol/L) had no effect on the percentage of SA β-gal positive cells and the expression of SAHF, and the hallmarks decreased at the concentration of 25 and 50 μmol/L, reaching the minimum at 50 μmol/L, while the percentage of SA β-gal positive cells and the expression of SAHF increased at the concentration of 100 μmol/L. Furthermore, we found that both on protein and mRNA levels of SIRT1 in the Y+N+S50 group was significantly increased compared with that in Y+N group. In conclusion, NaHS delays senescence of HUVECs induced by NAM via upregulation of SIRT1 expression.     

Ferulic acid augments angiogenesis via VEGF,PDGF and HIF-1α

Therapeutic angiogenesis is critical to wound healing and ischemic diseases such as myocardial infarction and stroke. For development of therapeutic agents, a search for new angiogenic agents is the key. Ferulic acid, a phytochemical found in many fruits and vegetables, exhibits a broad range of therapeutic effects on human diseases, including diabetes and cancer. This study investigated the augmenting effect of ferulic acid on angiogenesis through functional modulation of endothelial cells. Through endothelial cell migration and tube formation assays, ferulic acid (10^?6–10^?4 M) was found to induce significant angiogenesis in human umbilical vein endothelial cells (HUVECs) in vitro without cytotoxicity. With chorioallantoic membrane assay, ferulic acid (10^?6–10^?5 M) was also found to promote neovascularization in vivo. Using Western blot analysis and quantitative real-time polymerase chain reaction, we found that ferulic acid increased vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) expression in HUVECs. Furthermore, the amounts of hypoxic-induced factor (HIF) 1α mRNA and protein, the major regulator of VEGF and PDGF, also showed up-regulation by ferulic acid. Electrophoretic migration shift assay showed that the binding activity of HIF-1α was also enhanced with ferulic acid treatment of HUVECs. Moreover, inhibitors of extracellular-signal-regulated kinase 1/2 and phosphoinositide-3 kinase (PI3K) abolished the binding activity of HIF-1α and the subsequent activation of VEGF and PDGF production by ferulic acid. Thus, both mitogen-activated protein kinase and PI3K pathways were involved in the angiogenic effects of ferulic acid. Taken together, ferulic acid serves as an angiogenic agent to augment angiogenesis both in vitro and in vivo. This effect might be observed through the modulation of VEGF, PDGF and HIF-1α.     

Synchronous fluorescence determination of ferulic acid with Ce(IV) and sodium tripolyphosphate

In this study, a synchronous fluorescence detection method for ferulic acid (FA) is proposed based on a redox reaction between FA and Ce(IV) sulfate in dilute sulfuric acid medium at room temperature. It was found that FA could reduce Ce(IV) to Ce(III) in acidic medium, and sodium tripolyphosphate could further enhance the intrinsic fluorescence of the Ce(III) produced. The enhanced extent of synchronous fluorescence intensity was in proportion to the concentration of FA over the range 3.0 × 10^‐8 to 1.0 × 10^‐5 mol/L. The corresponding limit of determination (S/N = 3) was 1.3 × 10^‐8 mol/L. The proposed method was applied to the determination of sodium ferulate for injection sample with satisfactory results. Copyright © 2013 John Wiley & Sons, Ltd.     

Control of Negative Gravitropism and Tension Wood Formation by Gibberellic Acid and Indole Acetic Acid in Fraxinus mandshurica Rupr. var. japonica Maxim Seedlings

In the present study, we investigated the role of gibberellic acid (GA3) and indole acetic acid (IAA) in the gravity response of stems and tension wood formation using two-year-old stems of Fraxinus mandshurica Rupr. var.japonica Maxim seedlings. Forty-five seedlings were used and divided into nine groups that included five seedlings in each group. Seedlings were treated with applications of GA3 alone at concentrations of 2.89 × 10-8and 2.89 × 10-7 μmol/L, IAA alone at concentrations of 5.71×10-8 and 5.71 ×10-7 μmol/L, or their combination to the apical bud of the stem using a micropipette. Seedlings were positioned horizontally after the first treatment.The same treatments were repeated six times per week. At the end of the experiment, all seedlings were harvested. Then, stem segments were cut under a light microscope. Application of exogenous GA3 at the higher concentration stimulated the upward bending of stems, whereas exogenous IAA had no effect. A synergistic effect of GA3 and IAA on upward stem bending was observed following application of the two combinations of GA3 and IAA. Moreover, application of exogenous GA3 at the higher dose stimulated wood formation on both the upper and lower sides of the stems, whereas the mixture of GA3 and IAA had a synergistic effect on wood formation in horizontal stems. Application of exogenous IAA alone at the lower concentration (5.71×10-8 μ mol/L) or application of a mixture of the higher concentrations of GA3 (2.89 × 10-7 μmol/L) and IAA (5.71×10-7 μmol/L) inhibited the development of gelatinous fibers (the G-layer) of tension wood on the upper side of the horizontal stems. The differentiation of gelatinous fibers of tension wood was not inhibited by GA3when it was applied alone, whereas the development of the gelatinous fibers of tension wood was strongly affected by the application of IAA. The findings of the present study suggest that the development of the G-layer is not related to the dose of GA3, but needs a relatively lower concentration of IAA.     

血管钠肽抑制低氧刺激心脏成纤维细胞增殖的机制研究

目的：研究血管钠肽（VNP）抑制低氧刺激的心脏成纤维细胞增殖的机制。方法：发离、培养乳鼠心脏成纤维细胞,随机分为四组：对照组、低氧组、低氧＋VNP组和低氧＋8－Bromo-cGMP组。以MTT法观察各组细胞的生长情况,分别采用放射免疫和免疫组化的方法研究了VNP对细胞内cGMP水平和增殖细胞核抗原（PCNA）表达的影响。结果：低氧24h可以使培养的乳鼠心脏成纤维细胞MTT A490nm值显著升高（P＜0．05vs对照组）,VNP（10^-7mol/L和8－Bromo-cGMP(10^-3mol/L)均可以显著降低低氧刺激的心脏成纤维细胞MTT A490nm值（P＜0．05vs低氧组）;对照组和低氧组细胞内cGMP水平无显著差异,而VNP（10^-7mol/L）能升高细胞内cGMP水平（P＜0．05vs对照组、低氧组）;低氧组PCNA的表达显著强于对照组（P＜0．05vs对照组）,VNP（10^-7mol/L可以使低氧刺激的心脏成纤维细胞PCNA表达减弱（P＜0．05vs低氧组）。结论：VNP抑制低氧刺激的心脏成纤维细胞增殖与升高细胞内cGMP水平、减弱PCNA的表达有关。     

全反式维甲酸抑制猪脂肪间充质干细胞的成脂分化

分离培养猪脂肪间充质干细胞（adipose mesenchymal stem cells, AMSCs）,流式细胞仪鉴定其表面标记.利用MTT比色检测不同浓度的全反式维甲酸（all trans retinoic acid, ATRA）对猪AMSCs增殖的影响;光学显微镜下观察猪AMSCs向脂肪细胞分化的形态学变化;油红O染色提取法分析不同浓度ATRA对猪AMSCs成脂分化的影响;RT PCR检测脂肪细胞分化标志基因LPL和aP2 mRNA的变化.MTT比色结果显示,生理浓度（1×10^－9～1×10^－8 mol/L）和药理浓度（1×10^－7～1×10^－5 mol/L）ATRA对猪AMSCs增殖均没有影响.油红O染色提取法结果表明,除1×10^－7　mol/L ATRA对猪AMSCs成脂分化没有影响外,生理浓度（1×10^－9～1×10^－8 mol/L）和其它药理浓度（1×10^－6～1×10^－5 mol/L）ATRA均显著抑制猪AMSCs成脂分化（P<0.05）.RT-PCR检测显示,ATRA显著抑制脂肪细胞分化标志基因LPL和aP2 mRNA表达（P<0.05）.     

His-tag的人胞浆磷脂酶A_2的C2结构域的表达、纯化及性质

带有His tag的人胞浆磷脂酶A2 的C2结构域高效表达 ,用内源荧光的变化测定了其稳定性和其与钙离子结合的结合常数 .结果表明 ,带有His tag的C2结构域仍可有效用于研究其折叠及其与钙离子的协同性结合 ,温度从 2 2℃升高到 35℃时 ,C2结构域和钙离子结合的协同性程度显著增强 .     

纳米金生物条形码技术检测痕量二噁英类化合物

建立一种基于纳米金生物条形码技术的二噁英快速筛检方法.利用二噁英诱 导激活的芳香烃受体复合物,特异识别以纳米金为报告基团的二噁英反应探针,该 探针被释放后进行条形码放大,通过纳米金银染技术增强识别信号,并记录其吸光度值,从 而可以简单灵敏地快速筛检二噁英类化合物.在一定的反应时间和浓度范围内（10^-14～10^-10mol/L）,溶液的吸光度值与2,3,7,8 四氯二苯并二噁英（2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD）浓度之间呈正相关 ,方法检测限为0.01 pmol/L,变异系数为5%～8%.用纳米金生物条形码（Nano Barcod e,nanoparticle based bio barcode）方法和现有的生物分析方法（CALUX,chemical activated luciferase gene expression）分别测定TCDD标准品,并绘制剂量效应曲线.结 果表明,本方法灵敏度高,线性范围宽,重复性好.本研究纳米金生物条形码方法的检测灵 敏度高于CALUX将近5倍(EC₅₀分别为 4×10^-12 mol/L 和 2×10^{- 11} mol /L),检测限较CALUX降低了10倍（检测限分别为1×10^-14 mol/L 和1×10 ^-13 mol/L）,变异系数分别为5%～8%和15%～30%.