乙肝病毒X蛋白对CCL13细胞Period1基因启动子甲基化及其表达的影响

目的 探讨乙肝病毒X蛋白(HBx)表达与肝细胞Period1基因低表达的关系及其机制。方法 采用脂质体法将pcDNA3.1-HBx质粒转入CCL13细胞,采用甲基化聚合酶链式反应(PCR)、反转录PCR(RT-PCR)、蛋白质印迹法(western blot)检测CCL13细胞转染HBx质粒前后Period1基因启动子甲基化水平、mRNA及蛋白表达水平。结果 pcDNA3.1-HBx质粒转染CCL13细胞后在该细胞中稳定表达,转染HBx质粒后,Period 1在CCL13细胞启动子甲基化水平较转染空质粒CCL13细胞明显增高,其mRNA及蛋白质的表达水平均较后者明显下降。结论 HBx蛋白可通过上调肝细胞Period1启动子甲基化水平,促使其表达下调。     

酪丝缬肽诱导高转移性肝癌细胞HCCLM3凋亡及机制研究

目的：观察酪丝缬肽（tyroservatide,YSV）诱导高转移性人肝癌细胞HCCLM3的凋亡,分析YSV对肿瘤细胞凋亡相关基因Bax与Bcl-2的影响。方法：建立人肝癌细胞HCCLM3的体外培养体系,用四甲基偶氮唑蓝比色法检测YSV对体外培养的HCCLM3的增殖抑制作用,流式细胞仪检测对照组与YSV剂量组的凋亡率,实时定量PCR法检测YSV对肝癌细胞中Bax与Bcl-2 mRNA表达,Western blotting检测YSV对Bax与Bcl-2蛋白表达的影响。结果：YSV可显著地抑制肝癌细胞HCCLM3的生长,当药物剂量10mg·L-1,作用72h时,抑制率为41.34%（P〈0.05）。YSV不同浓度组随着药物作用时间的延长肝癌细胞凋亡率呈升高趋势。实时定量PCR结果显示YSV能上调促凋亡基因Bax mRNA的表达,同时下调凋亡抑制基因Bcl-2 mRNA的表达。Western blotting在蛋白水平上进一步证实了实时定量PCR的结果。结论：YSV可在基因及蛋白水平上调促凋亡基因Bax的表达,同时下调凋亡抑制基因Bcl-2的表达,进而实现其诱导肝癌细胞HCCLM3的凋亡。     

p38信号通路对缺氧下大鼠星形胶质细胞增殖凋亡的影响及机制研究

目的探讨p38信号通路对缺氧下星形胶质细胞增殖凋亡的影响。方法从新生2 d的大鼠的脑组织分离原代星形胶质细胞,将细胞分为缺氧组、缺氧+p38抑制剂组和正常组,各组细胞培养12 h后,Western blot检测细胞中p38、p-p38蛋白表达;24 h后CCK8实验和流式细胞术分别检测细胞的增殖及凋亡情况,Western blot检测Bcl-2、Bax、Cleaved Caspase3蛋白表达。结果缺氧组p-p38蛋白表达显著高于正常组,而缺氧+SB203580组p-p38蛋白表达显著低于缺氧组(P0.01);缺氧组细胞存活率及Bcl-2蛋白表达均显著低于正常组,细胞凋亡率及Bax、Cleaved Caspase3蛋白表达均显著高于正常组(P0.01);缺氧+SB203580组细胞存活率及Bcl-2蛋白表达均显著高于缺氧组,细胞凋亡率及Bax、Cleaved Caspase3蛋白表达均显著低于缺氧组(P0.01)。结论 p38信号通路的激活降低了缺氧下星形胶质细胞增殖并促进细胞的凋亡,而抑制p38信号通路可提高细胞的增殖及抑制细胞的凋亡。     

活化蛋白C抑制血管内皮细胞凋亡的机制研究

目的 观察活化蛋白C(activated protein C,APC)对线粒体凋亡途径相关调节因子的影响,以阐述其抑制血管内皮细胞凋亡作用的可能机制.方法 人脐静脉血管内皮细胞与脂多糖(1μg/mL)孵育诱导细胞凋亡模型后,分别给予APC(10 ng/mL或50 ng/mL)建立药物治疗组,另设立对照和凋亡模型组,24 h后取材,RT-PCR和Western blotting检测Bcl-2,Bax,P53和Caspase 3 mRNA及蛋白表达.结果 不同剂量APC治疗组与凋亡模型组比较P53,Bax和Caspase 3 mRNA和蛋白表达下调,Bcl-2 mRNA和蛋白表达上调,尤以APC 50 ng/mL治疗组为显著(P<0.05).结论 APC可能参与调节Caspase 3依赖性的线粒体凋亡途径相关因子的表达,发挥抑制LPS诱导的血管内皮细胞凋亡,从而为APC制剂在感染性疾病中的使用提供了理论基础.     

沉默miR-21对子宫内膜癌顺铂耐药细胞株Ishikawa/DDP的影响

目的:观察沉默miR-21对子宫内膜癌顺铂耐药细胞株Ishikawa/DDP的影响。方法:以Lipofectamine 2000介导miR-21抑制剂转染Ishikawa/DDP细胞株,同时设置阴性组和耐药组。采用反转录PCR检测miR-21、多药耐药基因MDR1、促凋亡基因Bax和抗凋亡基因Bcl-2的表达。采用蛋白印迹法检测多药耐药蛋白P-gp、促凋亡蛋白Bax和抗凋亡蛋白Bcl-2的表达。采用噻唑蓝比色法检测细胞对顺铂的敏感性。采用流式细胞术检测细胞凋亡情况。结果:与耐药组和阴性组比较,抑制剂组miR-21,MDR1和Bcl-2mRNA表达显著下调(P0.01),而Bax mRAN表达显著上调(P0.001);抑制剂组P-gp和Bcl-2蛋白表达显著低下调(P0.05),而Bax蛋白表达显著上调(P0.001)。与耐药组和阴性组比较,顺铂对抑制剂组的IC50值显著(P0.001);顺铂对抑制剂组细胞的诱导凋亡率显著增加(P0.001)。结论:沉默miR-21可显著提高Ishikawa/DDP细胞株对顺铂的敏感性,并促进细胞凋亡,其具体机制可能与下调MDR1,P-gp和Bcl-2表达,以及上调Bax表达有关。     

缺氧环境中胸腺素β4基因转染骨髓间充质干细胞凋亡率及Bax和Bcl-2的表达

背景：研究表明体外培养细胞加入胸腺素β4能增加细胞的抗凋亡能力,若在缺氧环境中上调胸腺素β4基因在骨髓间充干细胞中的表达,其抗凋亡能力如何改变,目前鲜见报道。
　　目的：观察胸腺素β4基因修饰的骨髓间充质干细胞在缺氧环境中的凋亡率改变,并探讨其是否通过调控Bax、Bcl-2表达影响凋亡能力。
　　方法：将携带有胸腺素β4基因的慢病毒转染骨髓间充质干细胞,转染完毕后利用Western blot法检测胸腺素β4在骨髓间充质干细胞中的表达。将细胞分为胸腺素β4转染组、对照病毒组、未转染组,分别置于缺氧环境中。流式细胞仪检测3组细胞凋亡率;Western blot法检测3组细胞中Bax和Bcl-2蛋白表达情况。
　　结果与结论：Western blot检测结果示,胸腺素β4基因在骨髓间充质干细胞中成功表达。流式细胞仪结果示,胸腺素β4转染组细胞凋亡率较对照病毒组、未转染组低,而对照病毒组、未转染组凋亡率差异无显著性意义。Western blot结果显示,Bcl-2蛋白在胸腺素β4转染组中表达量较对照病毒组、未转染组高,Bax蛋白在胸腺素β4转染组表达量较对照病毒组、未转染组低,而对照病毒组、未转染组中Bax、Bcl-2表达差异无显著性意义。提示过表达胸腺素β4基因可增加骨髓间充质干细胞在缺氧环境中的抗凋亡能力,其可能的作用机制是调控Bax和Bcl-2蛋白表达水平。     

碱性成纤维细胞生长因子荧光真核表达载体构建及对过氧化氢诱导血管内皮细胞凋亡的影响

背景：已证实外源性碱性成纤维细胞生长因子（basic fibroblast growth factor,bFGF）可抑制血管内皮细胞凋亡。目的：构建表达bFGF的荧光真核表达载体,探讨其对过氧化氢（H2O2）诱导的血管内皮细胞凋亡和凋亡相关蛋白的影响。方法：通过基因亚克隆构建荧光真核表达载体pcDNA3.1-bFGF-GFP,利用脂质体介导将bFGF基因导入人脐静脉内皮细胞内,通过荧光观察和RT-PCR检测基因的表达。实验分为3组,对照组（转染pcDNA3.1）、过氧化氢组（转染pcDNA3.1＋H2O2）和bFGF转染＋过氧化氢组（转染pcDNA3.1-bFGF-GFP＋H2O2）,流式细胞术测定细胞凋亡率,Western blot检测caspase-3 P17活性亚单位和Bax蛋白表达。结果与结论：成功构建荧光真核表达载体pcDNA3.1-bFGF-GFP,该载体转染人脐静脉内皮细胞后,bFGF mRNA显著增加,并可观察到绿色荧光。与对照组相比,过氧化氢组细胞凋亡率和caspase-3 P17活性亚单位、Bax蛋白的表达量都明显增加（P〈0.01）,而bFGF转染＋过氧化氢组的细胞凋亡率和caspase-3 P17活性亚单位、Bax蛋白的表达量则比过氧化氢组显著降低（P〈0.01）。证实bFGF基因转染能抑制过氧化氢诱导的血管内皮细胞凋亡,其作用机制可能与调控Bax蛋白表达和caspase-3活性有关。     

碱性成纤维细胞生长因子荧光真核表达载体构建及对过氧化氢诱导血管内皮细胞凋亡的影响

背景:已证实外源性碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)可抑制血管内皮细胞凋亡。目的:构建表达bFGF的荧光真核表达载体,探讨其对过氧化氢(H2O2)诱导的血管内皮细胞凋亡和凋亡相关蛋白的影响。方法:通过基因亚克隆构建荧光真核表达载体pcDNA3.1-bFGF-GFP,利用脂质体介导将bFGF基因导入人脐静脉内皮细胞内,通过荧光观察和RT-PCR检测基因的表达。实验分为3组,对照组(转染pcDNA3.1)、过氧化氢组(转染pcDNA3.1+H2O2)和bFGF转染+过氧化氢组(转染pcDNA3.1-bFGF-GFP+H2O2),流式细胞术测定细胞凋亡率,Western blot检测caspase-3 P17活性亚单位和Bax蛋白表达。结果与结论:成功构建荧光真核表达载体pcDNA3.1-bFGF-GFP,该载体转染人脐静脉内皮细胞后,bFGF mRNA显著增加,并可观察到绿色荧光。与对照组相比,过氧化氢组细胞凋亡率和caspase-3 P17活性亚单位、Bax蛋白的表达量都明显增加(P<0.01),而bFGF转染+过氧化氢组的细胞凋亡率和caspase-3 P17活性亚单位、Bax蛋白的表达量则比过氧化氢组显著降低(P<0.01)。证实bFGF基因转染能抑制过氧化氢诱导的血管内皮细胞凋亡,其作用机制可能与调控Bax蛋白表达和caspase-3活性有关。     

肝细胞生长因子激活剂的抑制剂-1基因对宫颈癌细胞自噬及凋亡调控的影响

目的探讨肝细胞生长因子激活剂的抑制剂-1(hepatocyte growth factor activator inhibitor-1, HAI-1)基因对宫颈癌细胞自噬及凋亡调控的机制。方法对数生长期HeLa细胞分为转染组和对照组,转染组转染HAI-1质粒,对照组细胞正常培养。采用实时荧光定量PCR法检测2组细胞HAI-1 mRNA表达情况,采用AO染色和流式细胞术检测2组细胞自噬情况,采用ELISA检测2组细胞自噬相关因子LC3-Ⅱ、LC3-Ⅰ和Beclin-1蛋白水平,应用流式细胞仪检测2组细胞凋亡率,采用Western blot法检测细胞Bax和Bcl-2蛋白相对表达量。结果转染组细胞HAI-1 mRNA相对表达量(1.57±0.26)、AO细胞荧光强度(52.14±3.88)、LC3-Ⅱ蛋白[(3.42±0.85)μg/L]、Beclin-1蛋白[(14.69±1.96)μg/L]水平、细胞凋亡率[(86.75±6.42)%]、Bax蛋白相对表达量(1.24±0.13)和Bax/Bcl-2(7.75±0.83)高于对照组[0.48±0.09、5.47±0.32、(1.10±0.22)μg/L、(10.12±0.53)μg/L、(12.64±1.33)%、0.25±0.06、0.17±0.05)](P0.05),LC3-Ⅰ蛋白水平[(0.59±0.11)μg/L]、Bcl-2蛋白相对表达量(0.16±0.04)低于对照组[(3.26±0.82)μg/L、1.47±0.15](P0.05)。结论 HAI-1转染通过增加HeLa细胞中LC3-Ⅱ和Beclin-1蛋白表达,降低LC3-Ⅰ蛋白表达,提高Bax/Bcl-2来调节宫颈癌细胞的自噬和凋亡。     

saRNA调控p21基因表达对肝癌细胞的抑制作用

目的探讨RNA激活p21对肝癌Hep G2、Hep 3b和SMMC-7721细胞生长和侵袭力的影响。方法化学合成靶向p21的saRNA,将其转染肝癌细胞系Hep G2、Hep 3b和SMMC-7721,利用荧光定量RT-PCR和免疫印迹检测细胞中的p21表达水平,并MTT法检测细胞生长情况及划痕实验观察细胞侵袭能力的变化。结果 Hep G2、Hep3b和SMMC-7721细胞的p21 mRNA分别较对照组升高了6.6、7.1、6.1倍,p21蛋白表达水平分别升高了17.4、11.4、6.7倍。细胞转染后48 h时的细胞增长平均抑制率分别为47%、53%和55%;划痕实验显示转染组细胞迁移能力显著低于对照组(P0.01)。结论靶向p21的RNAa能抑制肝癌细胞的生长和侵袭力,p21可作为一个具有肝癌治疗应用价值的靶基因。     

Activated protein C

Summary.  Protein C is a vitamin K-dependent plasma protein zymogen whose genetic mild or severe deficiencies are linked with risk for venous thrombosis or neonatal purpura fulminans, respectively. Studies over past decades showed that activated protein C (APC) inactivates factors (F) Va and VIIIa to down-regulate thrombin generation. More recent basic and preclinical research on APC has characterized the direct cytoprotective effects of APC that involve gene expression profile alterations, anti-inflammatory and anti-apoptotic activities and endothelial barrier stabilization. These actions generally require endothelial cell protein C receptor (EPCR) and protease activated receptor-1. Because of these direct cytoprotective actions, APC reduces mortality in murine endotoxemia and severe sepsis models and provides neuroprotective benefits in murine ischemic stroke models. Furthermore, APC reduces mortality in patients with severe sepsis (PROWESS clinical trial). Although much remains to be clarified about mechanisms for APC's direct effects on various cell types, it is clear that APC's molecular features that determine its antithrombotic action are partially distinct from those providing cytoprotective actions because we have engineered recombinant APC variants with selective reduction or retention of either anticoagulant or cytoprotective activities. Such APC variants can provide relatively enhanced levels of either cytoprotective or anticoagulant activities for various therapeutic applications. We speculate that APC variants with reduced anticoagulant action but normal cytoprotective actions hold the promise of reducing bleeding risk because of attenuated anticoagulant activity while reducing mortality based on direct cytoprotective effects on cells.     

Significance of lipopolysaccharide-binding protein (an acute phase protein) in monitoring critically ill patients

Introduction  

The present study was conducted to assess the value of serum concentration of lipopolysaccharide-binding protein (LBP) in patients with systemic inflammatory response syndrome (SIRS), sepsis and septic shock with respect to its ability to differentiate between infectious and noninfectious etiologies in SIRS and to predict prognosis.     

The diagnostic value of urine heat shock protein 70 and prostatic exosomal protein in chronic prostatitis

ObjectiveTo explore the diagnostic value of the levels of prostatic exosomal protein (PSEP) and heat shock protein 70 (HSP70) in the urine of patients with chronic prostatitis (CP).MethodUrine samples from 210 CP patients (70 cases of the USA National Institutes of Health Category II [NIH‐II], 70 NIH‐IIIa, and 70 NIH‐IIIb patients) and 70 control subjects were collected between May 2018 and February 2020. The levels of PSEP and HSP70 in urine were detected by enzyme‐linked immunosorbent assay. The differences in urine PSEP and HSP70 levels between the groups were analyzed, and receiver operating characteristic (ROC) curves were used to analyze the clinical value of PSEP and HSP70 in the diagnosis of CP.ResultsThe PSEP levels of CP patients were significantly higher than those of the control group (p < 0.001), but there was no difference in PSEP levels among CP subgroups. The level of HSP70 in the urine of the NIH‐II patients was significantly lower than the levels in the NIH‐IIIa and NIH‐IIIb subgroups and the control group, but there was no difference in HSP70 levels between the NIH‐IIIa and NIH‐IIIb subgroups and the control group. ROC curve analysis results showed that the area under the curve (AUC) of PSEP for the NIH‐II, NIH‐IIIa, and NIH‐IIIb patients was 0.751, 0.776, and 0.731, respectively. The AUC of HSP70 in NIH‐II patients was 0.784, and the AUC of combined detection of PSEP and HSP70 in NIH‐II patients was 0.858.ConclusionUrine PSEP can be used as a marker for the diagnosis of CP, but it cannot distinguish between the various types of CP, and HSP70 can be used as a diagnostic index for NIH‐II classification.     

贲门癌变过程中Survivin和Cyclin-E蛋白的表达及相关性研究

目的检测Survivin蛋白和Cyclin-E蛋白在贲门癌和癌前病变中的表达变化,探讨两者表达的相关性。方法应用免疫组化SP法检测Survivin蛋白和Cyclin-E蛋白在贲门癌和癌前病变组织中的表达变化,分析两者在不同程度贲门病变组织中表达的相关性。结果①从贲门炎到腺上皮不典型增生(Ⅰ、Ⅱ、Ⅲ级)到贲门癌,Survivin蛋白和Cyclin-E蛋白表达均呈逐渐增高趋势,Survivin蛋白的表达率高于Cyclin-E蛋白。②两者在Ⅲ级不典型增生组中的表达与贲门癌组比较差异无显著性(P>0.05)。③Survivin蛋白和Cyclin-E蛋白在贲门未分化腺癌组中表达均高于其在低分化、高分化腺癌组中表达,组间差异有显著性(P<0.01)。④Survivin蛋白和Cyclin-E蛋白在贲门炎、腺上皮不典型增生(Ⅰ、Ⅱ、Ⅲ级)和贲门癌中的表达呈正相关(r=0.881,P<0.05)。结论在贲门不同病变组织中Survivin蛋白和Cyclin-E蛋白表达随着病变严重程度和恶性程度的增高而增高;两者在贲门癌及癌前病变的发生发展过程中起协同作用,共同抑制细胞凋亡、促进细胞增殖。     

噬菌体展示技术筛选人肠道病毒71型3A 蛋白相互作用蛋白

目的：利用 T7噬菌体展示技术筛选与人肠道病毒71型3A 蛋白相互作用的蛋白。方法构建3A 蛋白的原核表达载体,表达并纯化3A 蛋白,以3A 蛋白为靶蛋白,应用 T7噬菌体展示技术对人肝细胞 cDNA 文库进行筛选,对筛选到产物进行DNA 序列分析及同源性研究。结果表达并纯化了3A 蛋白,经过4轮筛选后,选择37个阳性克隆,采用 T7特异性引物扩增插入片段,将 PCR 产物送公司进行测序。经过同源性分析,确定了2个与人肠道病毒3A 蛋白相互作用蛋白。结论通过 T7噬菌体展示技术可以得到与3A 蛋白相互作用蛋白,通过研究此蛋白的功能就可以初步推测出3A 蛋白可能的功能,为进一步研究人肠道病毒的致病机制鉴定了基础。     

Comparison between C-reactive protein and adipocyte fatty acid-binding protein as a component of metabolic syndrome in middle-aged women

Objectives

We compared the diagnostic accuracy of CRP and adipocyte fatty acid-binding protein (A-FABP) for the metabolic syndrome (MS).

Design and methods

We examined 310 middle-aged Caucasian women.

Results

CRP and AFABP values were significantly associated with the MS probability in the logistic regression model. Operating characteristic curves comparison showed similar areas under the curve.

Conclusions

Measurement of A-FABP is equivalent to CRP in the diagnostic utility of the MS.     

血清高敏C反应蛋白及S100B蛋白与脑出血关系的研究

目的 探讨血清高敏C反应蛋白(hs-CRP)及S100B蛋白水平与脑出血病情、出血量及预后的关系.方法 对脑出血患者155例分型,用免疫透射比浊法测定hs-CRP含量,用双抗体夹心ELISA法测S100B蛋白含量,观察二者水平与脑出血病情、出血量及预后的关系.结果 ①腩出血病情愈重,血清hs-CRP及S100B蛋白含量愈高(P<0.01);②脑出血患者出血量愈多,ks-CRP及S100B蛋白含量愈高(P<0.01);③hs-CRP及S100B过高者,脑出血预后不良.④hs-CRP及S100B水平呈正相关(r=0.7,P=0.001).结论hs-CRP及S100B水平是判断脑出血患者病情和预后的良好监测指标.     

C-reactive protein as an indicator of sepsis

Objective: To determine the use of plasma C-reactive protein (CRP) concentrations, body temperature (BT) and white blood cell count (WBC) in the detection of sepsis in critically ill patients. Design: All patients admitted for more than 24 h in the intensive care unit (ICU) were prospectively included. Patients were followed up to ICU discharge and each patient-day was classified in one of four categories according to the infectious status: 1) Negative, patient-day without systemic inflammatory response syndrome (SIRS); 2) Definite, patient-day with SIRS and a positive culture; 3) SIRS, patient-day with SIRS and negative or no cultures. The last group was subdivided according to the following criteria: a) new, or persistence of, pulmonary infiltrates, b) the presence of pus in a place known to be sterile. Patient-days without these criteria were classified as SIRS with improbable sepsis (Unlikely), and with one criteria or more as SIRS with probable sepsis (Probable). Setting: Medical/surgical intensive care unit. Patients: Twenty-three patients were followed. Measurements and results: A total of 306 patient-days were analysed: 20 Negative, 15 Definite, 63 Unlikely and 208 Probable. The median (range) CRP values for Negative, Unlikely, Probable and Definite groups were as follows: 24.5 (7–86), 34 (5–107), 143 (39–544), and 148 (52–320) mg/l. The plasma CRP levels were significantly related to the infectious status (Negative, Unlikely, Probable or Definite) of the patient-day classification (p < 0.05). Concentrations of CRP in the Negative and Unlikely groups were significantly lower than in the Probable and Definite ones (p < 0.05). A plasma CRP of 50 mg/l or more was highly suggestive of sepsis (sensitivity 98.5 %, specificity 75 %). Conclusions: Daily measurement of CRP is useful in the detection of sepsis and it is more sensitive than the currently used markers, such as BT and WBC. Received: 22 December 1997 Accepted: 8 July 1998     

蛋白芯片用于筛选急性髓系白血病患者血清标志物的初步研究

目的利用生物素标记蛋白芯片筛选急性髓系白血病(AML)患者血清中可用于AML早期诊断、预后判断的血清标志物。方法采用生物素标记抗体芯片技术,对11名不同细胞遗传学和分子生物学特征的AML患者[分为预后良好组(5名),预后不良组(6名)]和5名健康体检者(对照组)的血清检测,采用芯片分析软件提取数据,获得的数据采用AAH-BLG-1数据分析软件作统计分析。结果 2个AML组与正常对照组相比,生长因子MFG-E8、osteoactivin、Hepassocin、M-CSF、M-CSF R、Insulin R,白细胞介素家族的IL-20、IL-3、IL-1 F8、IL-2 R alpha、IL-2 R beta、IL-1 R6凋亡因子(Fas)、粘附因子(ICAM-3)、趋化因子(CCL21)、载脂蛋白(Lipocalin-1)、跨膜蛋白(TMEFF1)、基质金属蛋白酶(MMP-3)和肿瘤坏死因子受体超家族的GFR alpha-4、TNF-alpha、TNFRF18、TNFRSF21等22个标志因子水平明显上调(P<0.05);预后不良组与预后良好组相比,IL-17RD、VEGF-D、IGFBP1、基质金属蛋白酶抑制剂TIMP-2、血管生成抑制剂Endostatin、蛋白水解酶uPA、趋化因子MIP-2、FGF-19、结合蛋白LBP、粘附分子L-selectin、载脂蛋白SAA等11个标志因子水平明显上调(P<0.05)。结论生物素蛋白质芯片共检测出33个AML血清标志物,证实这些标志物参与了AML细胞趋化、黏附、迁移、降解基质、恶性增殖、抗凋亡等过程。蛋白芯片有助于早期正确判断AML患者的预后,指导不同强度的个体化治疗。