CD10

人类白细胞分化抗原系统中CD10又名急性原始淋巴细胞白血病细胞共同抗原(Common acute Lymphoblastic Leukemia antigen, CALLA).Letarte等证实CD10就是一种与细胞膜缔合的中性内肽酶(neutral endopeptidase, NEP)或名脑啡肽酶(enkephalinase A).该酶以锌离子作辅基,能被EDTA、磷酰胺(Phosphoramidon)所抑制,故是一种金属酶,能水解疏水性氮基酸的α-氨基所形成的肽键,产生以苯丙氨酸(phe)、缬氨酸(Val)或酪氨酸(Tyr)为第一位残基的多肽.能被NEP水解的底物有脑啡肽、缓激肽、血管紧张素Ⅰ/Ⅱ、神经降压肽、催产素、P物质、趋化肽(甲硫·亮·苯丙三肽,Fmlp)等.     

CD45RA/CD45RO研究进展

目的 CD45RA和CD45RO是白细胞共同抗原的两种异型。CD45RA＋和CIM5RO＋T淋巴细胞在表型、功能等各方面均不同，了解其亚群的变化可能有助于了解许多疾病的发病机制、临床状态及预后。     

哮喘患儿CD8+CD28+、CD8+CD28-T淋巴细胞检测及其临床意义

目的通过对哮喘患儿CD4、CD8和CD28的联合检测,探讨哮喘患儿淋巴细胞免疫功能状态及其临床意义.方法采用流式细胞术检测哮喘患儿外周血的总T细胞(CD3+)、辅助/诱导T淋巴细胞(CD4+)、抑制/细胞毒T淋巴细胞(CD8+)、细胞毒T细胞(CD8+CD28+)、抑制T细胞(CD8+CD28-).结果哮喘患儿组与对照组比较;CD3+、CD4+、CD8+CD28-细胞均低于对照组(P＜0.01,P＜0.05),CD8+CD28+细胞增高(P＜0.05),CD4+/CD8+比值、CD8+与对照组比较均无显著性差异(P＞0.05).结论哮喘患儿存在T淋巴细胞亚群免疫功能紊乱,而CD8+CD28+、CD8+CD28-T细胞失衡可能是导致机体免疫功能紊乱的主要因素.     

CD3、CD4、CD8检测与病毒性心肌炎的关系

我们对40名病毒性心肌炎患者进行CD3、CD4、CD8检测,现报告如下:1资料与方法1.1研究对象40例病毒性心肌炎(以下称心肌炎)病人均来自住院病人,男22例,女18例,年龄3~62岁,平均年龄32.5岁,病程4天~1个月。另选30名健康者作对照,年龄3~60岁,平均3l.5岁,男16例,女14例。1.2检测方法CD3、CD4、CD8用免疫组化APAAP法,试剂盒天津血研所提供。2结果两组CD3、CD4、CD8结果见表。两组比较心肌炎患者CD3阳性无明显差异,CD4阳性与CD4阳性/CD8阳性显著降低,CD8阳性明显升高,见表。3讨论正常情况下,体内辅助性T细胞(TH)与抑制性T细胞(TS)值…     

AIHA/Evans综合征CD80、CD86和CD4+CD25+调节性T细胞的研究

目的探讨自身免疫性溶血性贫血(AIHA)/Evans综合征(AIHA同时或相继发生免疫性血小板减少性紫癜)患者外周血淋巴细胞共刺激分子CD80、CD86和CD4+CD25+调节性T细胞的表达水平,初步探讨共刺激分子CD80、CD86和CD4+CD25+调节性T细胞在AIHA/Evans综合征细胞免疫功能紊乱中的机制及其意义。方法应用流式细胞术检测24例次AIHA/Evans综合征患者治疗前后外周血淋巴细胞CD80、CD86和CD4+CD25+调节性T细胞比例的变化,并与正常对照组相比较。结果 AIHA/Evans综合征患者治疗前后与正常对照组比较CD80比例水平均无明显变化(P>0.05);发作时CD86表达水平高于对照组和治疗缓解组,差异具有统计学意义(P<0.05);CD4+CD25+调节性T细胞表达水平在AIHA/Evans综合征发作患者中表达明显下降,差异具有高度统计学意义(P<0.01)。结论淋巴细胞共刺激因子CD86和CD4+CD25+调节性T细胞异常表达可能参与AIHA/Evans综合征细胞免疫功能紊乱方面的发病机制。     

CD4+ CD25+调节性T细胞

机体的免疫系统维持着对感染性抗原的反应和自身耐受的平衡,而对自身抗原产生免疫耐受则是防止发生自身免疫病的关键。阴性选择中的克隆清除、免疫无能和克隆忽略被认为是控制自身反应性T细胞的主要机制。近些年随着研究的深入,CD4^＋ CD25^＋调节性T细胞（Treg细胞）在维持自身耐受中的作用得到进一步的认识。     

CD28/CTLA-4与CD4+CD25+Treg相关研究进展

调节性T细胞是一类表型和功能特异的T细胞亚群,其中CD4 CD25 调节性T细胞是近年来被研究得较为深入的一个亚类,也最值得引起人们的关注。虽然有研究已经证实CD4 CD25 调节性T细胞能够抑制CD4 CD25-T细胞和CD8 T细胞的活化和增殖,但其具体的作用机制还不清楚,有研究表明CD28/CTLA-4对CD4 CD25 调节性T细胞的产生,维持和免疫抑制作用的发挥起重要作用,因此进一步明确CD28/CTLA-4与CD4 CD25 T细胞的关系有助于人们在临床免疫治疗中更好地了解和应用CD4 CD25 调节性T细胞。     

慢性乙型肝炎患者外周血CD80、CD86及其受体CD28的表达

目的研究慢性乙型肝炎患者外周血CD80、CD86及其受体CD28与其病情状态、乙型肝炎病毒复制的关系。方法用流式细胞术检测了24名健康体检者和92例慢性乙型肝炎患者外周血CD80、CD86、CD28的表达和CD8^＋CD28^＋、CD8^＋CD28^-亚群淋巴细胞,并与病毒载量和乙型肝炎e抗原（HBeAg）进行相关分析。结果慢性乙型肝炎CD80和CD86表达明显高于正常对照组和乙型肝炎病毒携带组（P〈0．01）;肝炎后肝硬化组明显高于慢性乙型肝炎组（P〈0．05）;慢性乙型肝炎轻、中、重度3组间差异也有统计学意义。慢性乙型肝炎组CD28的表达明显低于正常对照组和乙型肝炎病毒携带组（P〈0．05）。病毒载量高低和HBeAg是否阳性与外周血CD80、CD86、CD28及CD8^＋CD28^＋和CD8^＋CD28^-亚群淋巴细胞差异无统计学意义。结论CD80、CD86及受体CD28可能在慢性乙型肝炎免疫损伤过程中起重要作用,但与血清中病毒载量的变化和HBeAg阳性与否无关。     

CD55、CD59与再生障碍性贫血

<正>补体调节蛋白CD55、CD59与阵发性血红蛋白尿症(paroxysmal nocturnal hemoglobinuria,PNH)关系密切,CD55、CD59已被广泛应用于PNH诊断中[1],并将CD55、CD59表达缺乏的细胞称为PNH细胞。Ruiz-Delgado等[2]发现红细胞表面CD55、CD59     

普伐他汀调脂过程中P-选择素表达的变化

目的：探讨普伐他汀促进动脉粥样硬化斑块消退的机制。方法：观察高胆固醇血症患者经普伐他汀１０～２０ｍｇ／ｄ治疗４周及８周后血小板功能和血脂的变化。结果：治疗４周及８周后血胆固醇降低，同时每个血小板膜表面Ｐ选择素的分子数由治疗前的７４８±１５４分别降至４７８±１１０和３７８±１１９；血浆Ｐ选择素由治疗前的２４．３±９．９μｇ／Ｌ分别降至１６．８±４．５和１６．１±４．０μｇ／Ｌ，血小板膜表面和血浆Ｐ选择素之间显示较好的相关性（ｒ＝０．８７２２）。结论：普伐他汀促进动脉粥样硬化斑块消退的早期效益是由于对血小板功能的良性影响而产生。     

Oxidative stress-mediated platelet CD40 ligand upregulation in patients with hypercholesterolemia: effect of atorvastatin

OBJECTIVES: We speculated that in patients with hypercholesterolemia CD40L overexpression could depend on low-density lipoprotein (LDL)-induced enhanced intraplatelet formation of O(2)*(-) and statin could reduce platelet CD40L via interference with platelet O(2)*(-) production. BACKGROUND: CD40L is a protein with inflammatory and thrombotic properties. CD40L is upregulated in platelets from hypercholesterolemic (HC) patients but the underlying mechanism is unclear. METHODS: Collagen-induced platelet CD40L and platelet O(2)*(-) expression were investigated in 40 HC patients and 40 healthy subjects. HC patients were then randomized to either a diet (n = 20) (group A) or atorvastatin 10 mg day (n = 20) (group B); the above variables were measured at baseline and after 3 and 30 days of treatment. O(2)*(-) and CD40L were also measured in vitro in LDL-treated platelets with or without nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor or atorvastatin added. RESULTS: Compared with controls, HC patients showed higher values of platelet CD40L (P < 0.001) and O(2)*(-) (P < 0.001). Platelet CD40L was significantly correlated with O(2)*(-) (P < 0.001). The interventional trial showed no changes in group A and a significant and parallel decrease in platelet CD40L (P < 0.001) and O(2)*(-) (P < 0.001) in group B. In vitro studies demonstrated that LDL-induced platelet CD40L and GP IIb/IIIa (PAC1 binding) activation via the NADPH oxidase pathway. CD40L upregulation was counteracted by atorvastatin in a dose-dependent fashion. CONCLUSIONS: This study suggests that in patients with hypercholesterolemia platelet CD40L is upregulated via NADPH oxidase-dependent O(2)*(-) generation. Atorvastatin downregulated CD40L with an oxidative stress-mediated mechanism likely involving platelet NADPH oxidase, an effect that seemed to be independent of its cholesterol-lowering action.     

单独采集血小板和浓缩血小板在保存期中的活化情况

研究单独采集血小板 (单采血小板 )和浓缩血小板在保存期中的活化情况。用流式细胞术对这两种血小板的CD62 p和CD41表达量进行测定。结果表明 :在保存 0 ,1 ,3和 5天时 ,单采血小板的CD62 p阳性率和CD41的平均荧光强度分别为 (1 8 91± 6 2 5) % ,(1 9 48± 8 2 7) % ,(2 2 82± 6 0 6) % ,(56 71± 1 1 79) %及 (8 0 9±2 38) % ,(8 1 3± 2 45) % ,(8 44± 2 51 ) % ,(1 9 87± 6 1 3) % ,而浓缩血小板的分别为 (30 65± 1 2 33) % ,(31 46± 1 1 86) % ,(32 51± 1 3 0 5) % ,(63 55± 1 3 2 7) %及 (1 0 33± 4 37) % ,(1 1 0 9± 6 61 ) % ,(1 3 46± 9 69) % ,(2 4 41± 1 0 1 5) %。二项指标均随保存时间推移而上升。对这两种血小板的计数和 pH值测定显示 ,二者均随保存时间推移而下降。在保存 0 - 3天内两种血小板的计数 ,pH值 ,CD62 p和CD41表达量无显著差异。在第 5天血小板计数和pH值出现显著下降 (P <0 0 0 1 ) ;而CD62p和CD41表达量出现显著上升 (P <0 0 0 1 )。结论 :单采血小板优于浓缩血小板     

围术期胃癌患者血小板膜糖蛋白CD41、CD62P的变化

目的 :研究胃癌患者围术期血小板膜糖蛋白CD41、CD6 2P的变化 ,为围术期防凝抗凝提供理论依据。方法 :应用SDS -PAGE蛋白电泳和Westernblot(免疫印迹技术 )检测 2 6例胃癌患者围术期CD41、CD6 2P表达的变化。结果 :与正常人相比 ,胃癌患者CD41、CD6 2P含量增多 ,随着手术进行 ,两者含量进一步升高 ,尤以术后 30min为甚。结论 :胃癌患者术前血小板即处于活化状态 ,手术造成活化程度增强。因此 ,应注意围术期防凝抗凝措施 ,以防止血栓病的发生。     

Intravenous anesthesia inhibits leukocyte-endothelial interactions and expression of CD11b after hemorrhage

Hemorrhage increases adhesion of leukocytes to the venular endothelium, mediated by increased expression of the Mac-1 integrin complex (CD18/CD11b) present on leukocytes. Anesthetic agents may possess anti-inflammatory properties. Hence, this study determined the effects of i.v. anesthesia on leukocyte adhesion after hemorrhage in relation to expression of CD11b. METHODS: Male Wistar rats were (n = 57) anesthetized i.v. with propofol (Diprivan) and fentanyl, ketamine, or thiopental. During anesthesia, 10% of total blood volume was removed and intravital microscopy used to observe the rat mesentery and measure leukocyte (neutrophils) rolling and adhesion in postcapillary venules (15 - 25 microm). Flow cytometry was also used to determine CD11b expression on neutrophils from blood removed at the end of these experiments (n = 25) or blood incubated with anesthetic agents and activated with platelet activating factor ex vivo (0.1 micromol/L) (n = 24). RESULTS: Hemorrhage increased leukocyte adhesion (stationary count per 150 microm) in rats anesthetized with thiopental (baseline, 3.4 +/- 1.2; hemorrhage, 6.7 +/- 2.0; P < 0.05) but not in those receiving either ketamine (baseline, 3.6 +/- 1.3; hemorrhage, 3.3 +/- 1.3) or propofol/fentanyl (baseline, 6.2 +/- 2.0; hemorrhage, 5.8 +/- 0.8). Neutrophils collected from thiopental-treated rats had elevated CD11b expression with thiopental (mean fluorescence baseline, 67.5 +/- 1.3; hemorrhage, 83.6 +/- 5.3; P < 0.05) but not with propofol/fentanyl (mean fluorescence baseline, 69.1 +/- 1.3; hemorrhage, 65.9 +/- 1.6), and ketamine-treated rats (mean fluorescence baseline, 74.3 +/- 2.1; hemorrhage, 74.8 +/- 1.1). Ketamine also inhibited upregulation of CD11b with platelet activating factor ex vivo. CONCLUSIONS: After hemorrhage, leukocyte adhesion and CD11b expression increased during thiopental anesthesia, but propofol/fentanyl and ketamine protected against hemorrhage-induced leukocyte adhesion. The anti-inflammatory effect of ketamine was mediated by direct inhibition of CD11b expression on leukocytes.     

再生障碍性贫血患者CD4+ CD25+ CD127low调节性T细胞及Notch1表达水平的变化

目的 测定再生障碍性贫血(AA)患者治疗前后外周血CD4+ CD25+ CD127low调节性T细胞(Treg)的数量及叉头翼状螺旋转录因子(FOXP3)mRNA、Notch1 mRNA的表达水平,探讨Treg在AA发病中的作用及其机制.方法 流式细胞术检测29例初发AA患者、14例环孢素(CsA)治疗后恢复期及11例治疗后未恢复期患者外周血中CD4+ CD25+ CD127low T细胞、CD4+ CD25+ T细胞的数量,并与正常对照比较;采用RT-PCR检测FOXP3 mRNA和Notch1 mRNA的表达水平,分析两者相关性.结果AA初发组及治疗后未恢复组患者外周血中活化CD4+ CD25+ T细胞占CD4+ T细胞比例分别为(4.3±0.7)%、(4.2±0.6)%,明显高于正常对照组[(2.4±0.8)%](P＜0.05).CsA治疗后恢复组患者比例下降为(2.6±0.7)%(P＜0.05),与对照组比较差异无统计学意义.AA初发组及未恢复组CD4+ CD25+ CD127low T细胞在CD4+ T细胞中的比例分别为(2.4±1.2)%、(2.5±1.1)%,较正常对照组[(7.1±2.7)%]及恢复组[(5.3±1.0)%]明显降低(P值均＜0.01);但后两组比较差异无统计学意义.AA初发组患者FOXP3 mRNA及Notch1 mRNA分别为(0.260±0.011)和(0.018±0.005),较正常对照[(1.307±0.011)和(0.308±0.028)]表达明显下调(P值均＜0.01),治疗后分别为(1.287±0.012)和(0.281±0.013),表达较初发组显著提高(P值均＜0.01),与对照组比较差异无统计学意义(P值均＞0.05).AA患者CD4+ CD25+ CD127low T细胞、FOXP3均与Notch1表达呈正相关性(P值均＜0.01).结论AA患者外周血CD4+ CD25+ CD127low Treg减少,其抑制作用减弱,导致自身反应性T细胞过度活化,抑制造血.其作用机制之一可能与靶细胞表面Notch1分子表达降低相关.     

Expression of EMMPRIN (CD147) on circulating platelets in vivo

Summary. Background and Objectives: EMMPRIN (CD147) is a matrix metalloproteinase inducer present on leukocytes and recently identified on platelets in vitro. We examined platelet CD147 expression in vivo and in correlation with markers of platelet activation and coronary artery disease (CAD). Patients/Methods: This prospective observational study involved 70 subjects (55 patients with CAD and 15 controls). Platelet CD62P expression, PAC‐1 expression, platelet–leukocyte aggregates and CD147 (both platelet and leukocyte) expression were assessed by flow cytometry, and soluble CD62P expression was assessed by enzyme‐linked immunosorbent assay. A full blood count and high‐sensitivity C‐reactive protein test were performed. Results: CD147 was expressed on 20.45% ± 1.63% (mean ± standard error of the mean) of circulating platelets, whereas CD62P and PAC‐1 were expressed on 0.87% ± 0.12% and 0.90% ± 0.27% of platelets, respectively. Platelet CD147 expression correlated with CD62P expression (r = 0.359, P = 0.002), PAC‐1 expression (r = 0.428, P < 0.001), leukocyte CD147 expression (monocyte, r = 0.416, P = 0.001; granulocyte, r = 0.434, P < 0.001), C‐reactive protein level and neutrophil/lymphocyte ratio (NLR). CAD patients had significantly higher CD147 mean fluorescence intensity than controls on circulating platelets (2.41 ± 0.14 vs. 2.87 ± 0.09, P = 0.014), monocytes (8.57 ± 1.20 vs. 12.3 ± 0.57, P = 0.006) and granulocytes (4.30 ± 0.65 vs. 6.50 ± 0.34, P = 0.005). Age adjustment eliminated the association between platelet CD147 expression and CAD, but the association between leukocyte CD147 expression and CAD persisted. According to multivariate analysis, the independent predictors of platelet CD147 expression were monocyte CD147 expression, NLR and age. Conclusions: Platelet CD147 expression is evident in vivo and correlates moderately with traditional platelet activation markers and leukocyte CD147 expression. Platelet CD147 expression shows a stronger association with age, and leukocyte CD147 expression a stronger association with clinical CAD, suggesting differences in the regulation of platelet and leukocyte CD147 expression in vivo.     

妊娠高血压综合征患者外周血CD62P、CD63检测的临床意义

目的探讨妊娠高血压综合征(妊高征)患者、正常妊娠早期、中期、晚期妇女血小板活化状态、血小板指标、凝血功能指标的变化,探讨其对妊高征患者血栓前状态的临床预测及诊治价值。方法随机选取22例妊高征患者(妊高征组)、71例正常妊娠妇女(妊娠早期组24例、妊娠中期组23例、妊娠晚期组24例)和22例正常体检妇女(健康对照组)作为研究对象,运用流式细胞仪、血细胞分析仪、血凝仪观察各组血小板上CD62P、CD63的表达及血小板(PLT)、血小板压积(PCT)、血小板体积(MPV)、血小板宽度(PDW)、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(Fbg)等含量。结果妊高征组CD62P含量明显上调,与妊娠早期组、妊娠中期组和妊娠晚期组比较,差异具有统计学意义(分别P0.01、P0.01、P0.05);妊高征组CD63表达量也高于妊娠早期组、妊娠中期组及妊娠晚期组,但差异无统计学意义(P0.05)。妊娠晚期组CD62P表达量明显高于妊娠早期组及妊娠中期组,差异具有统计学意义(P0.01)。妊娠晚期组的PLT含量显著高于妊娠早期和妊娠中期组的孕妇(分别P0.01、P0.05)。妊高征组PLT含量减少,与妊娠早期组、妊娠中期组及妊娠晚期组相比差异无统计学意义(P0.05)。PLT与CD62P呈负相关(r=-0.256,P0.05);PLT与CD63呈负相关(r=-0.336,P0.01)。CD62P与CD63呈正相关(r=0.303,P0.01)。CD62P、CD63、PLT、MPV、PCT、PDW、PT、Fbg指标在妊娠晚期组、妊高征组和健康对照组之间差异有统计学意义(P0.01)。妊娠晚期组MPV、PDW、PT、Fbg与健康对照组相比明显上调,差异具有统计学意义(P0.01);TT与健康对照组相比明显下调,差异具有统计学意义(P0.01)。妊高征组CD62P、CD63、PDW、Fbg与健康对照组相比明显上调,差异具有统计学意义(P0.01);PLT、PCT与健康对照组相比明显下调,差异具有统计学意义(P0.01)。妊高征组CD62P与妊娠晚期组相比明显上调,差异具有统计学意义(P0.05);MPV、PCT、PT、Fbg指标与妊娠晚期组相比明显下调,差异具有统计学意义(P0.05)。联合检测CD62P和CD63诊断妊高征敏感性为77.3%,特异性为67.6%,假阳性率为32.4%,假阴性率为22.7%,阳性预测值为42.5%,阴性预测值为90.6%。结论流式细胞术检测CD62P、CD63比血小板和凝血功能指标更能反映血栓形成倾向,对妊高征的防治具有重要价值。     

Immunosuppressive therapy regimen and platelet activation in renal transplant patients

BACKGROUND: Increased platelet activation caused by an immunosuppressive therapy regimen may contribute to the high incidence of death from cardiovascular disease in renal transplant patients. Cyclosporine (INN, ciclosporin) and azathioprine are reported to activate platelets, but data are rare and controversial for tacrolimus and mycophenolate mofetil. METHODS: This cross-sectional study assessed markers of platelet degranulation (P-selectin; CD62), the activated glycoprotein IIb/IIIa receptor (PAC1, indicating the fibrinogen binding site), platelet aggregation, and secretion of platelet-derived growth factor (PDGF(AB)) in renal transplant patients treated with 4 different therapy regimens. Immunosuppression was based on low-dose steroids (5 mg/d prednisone) in combination with a single agent: (1) cyclosporine (n = 16), (2) azathioprine (n = 18), (3) tacrolimus (n = 17), or (4) mycophenolate mofetil (n = 13). Effects were compared with those in an age-matched control group of patients with hypertension (n = 11). RESULTS: In all renal transplant patient groups, unactivated platelets exhibited an increased expression of CD62. When stimulated with 2-micromol/L thrombin receptor-activating peptide, CD62 expression in platelets from patients treated with azathioprine (63% +/- 17%; P <.05), cyclosporine (51% +/- 23%; P <.05), and tacrolimus (50% +/- 22%; P <.05) was elevated compared with control subjects (33% +/- 19%). PAC1 expression was significantly increased in the patient groups that received azathioprine and cyclosporine. PDGF(AB) secretion was elevated in patients treated with azathioprine only (51 +/- 24 ng/10(9) platelets [versus 35 +/- 17 ng/10(9) platelets for control subjects]; P <.05). Platelet aggregation in response to collagen (0.5 microg/mL) was decreased in patients treated with tacrolimus (49% +/- 29%; P <.05) and mycophenolate mofetil (55% +/- 32%; P <.05) compared with control subjects (73% +/- 25%). CONCLUSION: This is the first study to compare the effects on platelet function of different immunosuppressive regimens that are based on monotherapy. All renal transplant patients showed preactivated platelets compared with those of patients with hypertension. However, the "newer" immunosuppressive agents tacrolimus and mycophenolate mofetil seemed to have fewer unfavorable effects on platelet CD62 expression and PAC1 expression and aggregation. Whether this finding is accompanied by fewer cardiovascular events remains to be elucidated.     

血管紧张素Ⅱ对脐血CD34+细胞体外分化为巨核细胞的影响

为了探讨血管紧张素Ⅱ对脐血CD34^＋细胞诱导分化为巨核细胞的影响，采用免疫磁珠法（MACS）分选8例健康产妇足月顺产胎儿脐血中的CD34^＋细胞，在舍血小板生成素（TPO50ng／ml）、白介素-3（IL-310ng／ml）、干细胞刺激因子（SCF50ng／l）的无血清培养液中添加浓度分别为50、100、1000μg／ml的血管紧张素Ⅱ作为实验组；同时以未添加血管紧张素Ⅱ的基础培养液作为对照组，培养14天后观察结果。细胞计数仪计数单个核细胞数（MNC）；流式细胞仪计数培养体系中的CD41^＋细胞数、血小板数，及分析细胞周期；利用CD41单克隆抗体免疫荧光染色观察培养体系中的细胞情况。结果表明：与对照组比较，实验组单个核细胞数无明显改变（P〉0．05）；而CD41^＋细胞和血小板数量有明显的增加（P〈0.05）；细胞周期分析显示，实验组的4倍体细胞增加，并存在明显的凋亡（P〈0．05）；荧光显微镜下观察对照组和实验组均可见大小不一的CD41^＋细胞。结论：血管紧张素Ⅱ可以促进脐血中CD34^＋细胞诱导分化为巨核细胞，并能促进巨核细胞产生血小板。