2型糖尿病外周血内皮祖细胞的诱导分化及影响因素的研究

目的观察2型糖尿病（T2DM）外周血内皮祖细胞（endothelial progenitor cell，EPC）在体外的分化增殖能力及影响因素。方法取20例T2DM无并发症患者、19例T2DM合并血管并发症患者和21例对照人群外周血EPC培养，观察细胞形态学变化并计数，用流式细胞仪检测贴壁细胞的特异性标志。结果糖尿病血管并发症组培养获得的EPC和EPC集落低于糖尿病无并发症组（P〈0．05）和对照组（P〈0．01）。EPC数量与SBP及FPG呈负相关（R=-0.266，P〈0.05；R=-0.619，P〈0．01），糖尿病人EPC集落生成数量与HbA1C水平呈负相关（R=-0．749，P〈0.05），与糖尿病病程年呈负相关（R=-0.406，P〈0．01）。结论FPG和SBP与EPC的增殖分化有关，T2DM外周血EPC数目减少，与HbA1c、SBP及病程相关。     

1型糖尿病患者外周血 CD4＋CD2＋5细胞数量及其对胰岛素治疗效果的影响

目的：探讨1型糖尿病（ T1DM）患者外周血中CD4＋CD2＋5调节性T细胞（以下简称CD4＋CD2＋5）在数量及对其胰岛素治疗效果的影响。方法采用流式细胞仪检测56例1型T1DM 患者（ T1DM 组）、43例2型糖尿病（T2DM）患者（T2DM组）及52例健康对照者（对照组）外周血中的CD4＋CD2＋5细胞比例,分析CD4＋CD2＋5比例与胰岛素治疗效果的关系。结果 T1DM组CD4＋CD2＋5比例显著低于其它两组P＜0．05）,且细胞比例越低,胰岛素治疗效果越差。结论 CD4＋CD2＋5在1型糖尿病患者外周血中呈低表达,可导致胰岛素的治疗效果下降。     

间日疟患者外周血NK γδ T Treg细胞含量的变化

目的 分析间日疟原虫现症感染者外周血中NK、γδ T细胞、CD4^＋CD25^＋T淋巴细胞及其FOXP3的表达情况，以初步了解患者的一些细胞免疫特性。方法用流式细胞仪检测25例间日疟原虫现症感染者（AC）、13例免疫对照者（IC）及14例正常对照者（NC）外周血中NK、γδT细胞和CD4^＋CD25^＋T淋巴细胞的百分含量，同时观察CD4^＋CD25^＋T细胞中表达FOXP3群体的百分含量。结果AC组外周血NK细胞百分含量为8．48％，与NC组（15．53％）及IC组（17．69％）比较，明显降低（P均〈0．05）,AC组外周血γδT细胞、CD4^＋CD25^＋T细胞百分含量分别为4．32％和5．42％，较NC组（2．55％和3．94％）及IC组（2．70％和3．44％）明显升高（P均〈0．05）；AC组外周血CD4^＋CD25^＋T淋巴细胞中表达FOXP3的细胞数量为8．14％，低于NC组的11．09％及IC组的11．32％，但差异无统计学意义（P〉0．05）。结论间日疟原虫急性感染期患者外周血NK细胞数量减少，但γδT淋巴细胞增加；CD4^＋CD25^＋T淋巴细胞中表达FOXP3群体的细胞稍有降低。     

慢性阻塞性肺疾病并2型糖尿病患者的免疫功能分析

目的观察慢性阻塞性肺疾病（COPD）并2型糖尿病（T2DM）患者的免疫功能,探讨其临床意义。方法选择COPD稳定期的患者60例,其中COPD合并T2DM患者30例、单纯COPD患者30例,健康对照组20例。检测外周血IgA、IgG、CD3^＋、CD4^＋、CD8^＋及CD4^＋/CD8^＋水平,并进行统计学分析。结果 COPD患者与健康对照组相比,外周血CD3^＋、CD4^＋、CD4^＋/CD8^＋、IgA、IgG、IgM均低,CD8^＋水平较高,差异有统计学意义（P〈0.05）;其中COPD合并T2DM患者与单纯COPD组相比,差异有统计学意义（P〈0.05）。结论 COPD并T2DM患者稳定期存在免疫功能异常,给予免疫干预治疗可能会减少COPD患者急性加重次数,改善预后。     

成人隐匿性自身免疫性糖尿病患者外周血T细胞亚群变化及意义

目的探讨T细胞亚群变化在成人隐匿性自身免疫性糖尿病（LADA）发病中的作用。方法应用流式细胞技术测定24例LADA患者（LADA组）、18例速发性1型糖尿病（T1DM）者（T1DM组）及20例健康人（对照组）T细胞表面分子CD4^＋、CD8^＋,以百分比表示各表面分子阳性T细胞占外周血淋巴细胞的比例;测定胰岛功能相关指标[空腹C肽（FC-P）和糖负荷后2h C肽（2h—CP）、胰岛素释放指数（HOMA-IS）]的相关性。结果LADA与T1DM组C1MT细胞、CD4^＋／CD8^＋值明显高于对照组（P〈0．01）,LADA与T1DM元显著差异。CD4^＋T细胞2h-CP呈明显负相关。结论T淋巴细胞亚群失衡参与介导了胰岛β细胞的损伤和LADA的发生,     

小儿重型肝炎患者外周血T淋巴细胞亚群的变化与临床意义

目的了解小儿与成人重型肝炎外周血CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量变化的差别,探讨小儿重型肝炎患者外周血T淋巴细胞亚群数量变化与临床意义。方法对35例小儿及30例成人重型肝炎进行外周血CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量检测。结果小儿重型肝炎成活的患儿外周血CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量明显高于死亡组（P〈0．01）：小儿重型肝炎中1岁以内患儿外周血CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量明显高于2～6岁组（P〈0．01）;小儿重型肝炎组CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量明显高于成人重型肝炎组（P〈0．01）;1岁以内的患儿病死率最高（P〈0．05）。结论／JxJL与成人重型肝炎外周血CD3^＋、CD3^＋CD4^＋及CD3^＋CD8^＋T淋巴细胞数量有明显差异,年龄越小,CD3^＋、CD3^＋CD4＋及CD3^＋CD8^＋T淋巴细胞数量越高;dxJL细胞免疫与成人明显不同,年龄越小,病情越重;病死率越高。     

1型糖尿病患者外周血中CD4^＋CD25^＋与CD8^＋CD28^-调节性T细胞水平的研究

流式细胞仪检测1型糖尿病（T1DM）患者外周血CD4^＋CD25^＋与CD8^＋CD28^-调节性T细胞的水平,发现其外周血CD4^＋CD25^＋T淋巴细胞水平[（2．02±0．43）％]显著低于2型糖尿病（T2DM）组[（6．79±1．75）％]和健康对照（NC）组[（7．84±1．45）％],而CD8^＋CD28^-调节性T细胞水平三组间无差异。     

干扰素α-2b联合利巴韦林治疗慢性丙型肝炎患者肝内免疫细胞的变化

目的观察干扰素α-2b和利巴韦林联合治疗前后漫性丙型肝炎患者肝内免疫细胞动态变化情况，为研究免疫调节疗法提供依据。方法利用流式细胞计数仪对42例慢性丙型肝炎患者应用联合治疗前及其中11例治疗后患者末梢血和（或）肝脏组织进行分析。结果与对照组相比慢性丙型肝炎组肝脏内CD56^＋、CD57^＋、CD161^＋细胞及CD56^＋T淋巴细胞阳性率明显减少（P〈0．01），CD161^＋T淋巴细胞有减少倾向；CD56^＋T淋巴细胞表达的CD28可见减少，CD152的表达可见增加（P〈0．05）；CD83^＋CD1a^＋细胞阳性率有减少倾向，CD80^＋CD11c^＋、CD86^＋CD11c^＋细胞阳性率明显减少（P〈0．01）；显效组减低的CD56^＋、CD161^＋、CD56T、CD161^＋T、CD80^＋CD11c^＋、CD86^＋CD11c^＋细胞治疗后可见增加。结论慢性丙型肝炎患者肝脏内自然杀伤细胞、自然杀伤T淋巴细胞数量及树突状细胞数量和功能减低，联合治疗使细胞免疫功能的抑制得到了改善。     

2型糖尿病患者外周血内皮祖细胞数量和功能的变化

目的观察2型糖尿病（DM）患者外周血内皮祖细胞（EPCs）数量和功能的改变。方法选择2型DM患者16例和对照组19例，密度梯度离心法收集外周血单个核细胞（MNCs），诱导分化培养7d后，荧光染色和流式细胞术分别鉴定贴壁细胞为EPCs。采用二苯基四氮唑嗅盐（MTT）比色法、黏附能力测定实验和体外血管生成实验检测EPCs的增殖能力、黏附能力和体外血管生成能力。结果2型DM患者外周血EPCs数量明显减少[（3．1±1．2）×10^5]：[（3．9±1．1）×10^5]，P〈0．05。且2型DM患者外周血EPCs黏附能力[（50±15）：（60±11）细膨×200视野，P〈0．05]，增殖能力[（0．170±0．056）：（0．225±0．071）OD值，P〈0．05]，体外血管生成能力均明显受损。结论2型DM患者外周血EPCs的数量减少，且其增殖、黏附和血管生成能力受损。     

强直性脊柱炎患者外周血CD4^＋CD25^＋CD127^low/-T细胞检测及其意义△

目的检测CD4^＋CD25^＋CD127^low/-T细胞在强直性脊柱炎（ankylosing spondylitis，AS）患者外周血的表达，并分析其与CD4^＋CD25^＋FOXP3^＋T细胞的相关性。方法 以21例AS患者外周血为研究组，20例类风湿关节炎（rheumatoid arthritis，RA）患者和24名正常人外周血作为对照组，采用三色直接荧光素标记法和多参数流式细胞仪检测外周血CD4^＋CD25^＋CD127^low/-T细胞、CD4^＋CD25^high细胞及CD4^＋CD25^＋FOXP3^＋T细胞的比例，同时检测外周血C反应蛋白（C-reactive protein，CRP）、血沉（ESR）、免疫球蛋白、补体等水平以及HLA—B27并进行相关性分析。结果与正常对照组相比，AS患者外周血CD4^＋CD25^＋CD127^low/-T及CD4^＋CD25^＋FOXP3＋T细胞百分率降低（均P〈0．05）。CD4^＋CD25^＋细胞百分率升高（P〈0．05）；CD4^＋CD25^＋CD127^low/-T细胞与CD4^＋CD25^＋FOXP3^＋T细胞呈正相关（r=0．589，P=0．021），与CRP、ESR、血小板及免疫球蛋白（IgG、IgA、IgM）和补体（C3、C4）、BASDAI、HLA-B27等均无明显相关性（均P〉0．05）。AS患者外周血CD4^＋CD25^＋CD127^low/-T细胞、CD4^＋CD25^＋FOXP3^＋T细胞和CD4＋CD25^highT细胞的百分率与RA患者外周血比较差异均无统计学意义（P〉0．05）。结论AS患者外周血CD4^＋CD25^＋CD127^low/-T细胞降低，且与CD4^＋CD25^＋FOXP3^＋T细胞呈正相关，提示在调节性T细胞研究中CD127具有替代FOXP3的可能性。     

黄芪多糖对2型糖尿病患者外周血内皮祖细胞增殖及NO生成的影响

目的观察黄芪多糖（APS）对2型糖尿病（T2DM）患者外周血内皮祖细胞（EPCs）增殖和NO生成的影响,并探讨其机制。方法密度梯度离心法获取外周血单个核细胞,培养7 d后鉴定EPCs,检测APS对T2DM组EPCs增殖的影响。观察APS对T2DM组EPCs NO浓度影响的时效和量效关系,然后予磷脂酰肌醇三磷酸激酶（PI3K）抑制剂LY294002和APS共培养,检测NO浓度。结果 APS在一定剂量和时间范围内能促进T2DM组EPCs增殖（P〈0.05）,并呈剂量和时间依赖性地升高EPCs NO浓度;PI3K抑制剂LY294002能阻断APS升高的NO水平（P〈0.05）。结论鼠尾胶原可代替EPCs培养中常用的纤维连接蛋白,是体外分离培养外周血EPCs更节省的一种方法。APS能促进EPCs增殖,并促进其NO的生成,PI3K抑制剂LY294002能阻断APS引起的NO的生成。     

Downregulation of microRNA-126 in endothelial progenitor cells from diabetes patients, impairs their functional properties, via target gene Spred-1

Diabetes mellitus (DM) adversely affects the number and function of circulating endothelial progenitor cells (EPCs). Consequently, there is also a reduction in the repair mechanism of these cells, which is a critical and initiating factor in the development of diabetic vascular disease. The aim of the present study was to analyze miR expression profiles in EPCs from patients with DM and choose the most significantly regulated miR to study its possible role on EPC dysfunction and elucidate its mechanism of action. EPCs were collected from subjects with Type II DM and non-diabetic control subjects. Total RNA was harvested from EPCs, and a total of 5 candidate miRNAs were identified by microarray screening and were quantified by TaqMan real-time PCR. Lentiviral vectors expressing miR-126 and miR-126 inhibitor (anti-miR-126) were transfected into EPCs, and the EPC colony-forming capacity, proliferation activity, migratory activity, differentiation capacity, and apoptotic susceptibility were determined and Western Blotting and mRNA real-time PCR analyses were performed. To study the mechanisms, lentiviral vectors expressing Spred-1 and a short interfering RNA (siRNA) targeting Spred-1 were prepared. Five miRs were aberrantly downregulated in EPCs from DM patients. These miRs included miR-126, miR-21, miR-27a, miR-27b and miR-130a. Anti-miR-126 inhibited EPC proliferation, migration, and enhanced apoptosis. Restored miR-126 expression in EPCs from DM promoted EPC proliferation, migration, and inhibited EPC apoptosis ability. Despite this, miR-126 had no effect on EPC differentiation. miR-126 overexpression significantly downregulated Spred-1 in EPCs. The knockdown of Spred-1 expression in EPCs from DM promoted proliferation, migration, and inhibited apoptosis of the cells. The signal pathway of miR-126 effecting on EPCs is partially mediated through Ras/ERK/VEGF and PI3K/Akt/eNOS regulation. This study provides the first evidence that miR-126 is downregulated in EPCs from diabetic patients, and impairs EPCs-mediated function via its target, Spred-1, and through Ras/ERK/VEGF and PI3K/Akt/eNOS signal pathway.     

Impaired development and dysfunction of endothelial progenitor cells in type 2 diabetic mice

AimDysfunction of circulating endothelial progenitor cells (EPCs) has been shown to affect the development of microvascular diseases in diabetes patients. The aim of this study was to elucidate the development and mechanical dysfunction of EPCs in type 2 diabetes (T2D).MethodsThe colony-forming capacity of EPCs and differentiation potential of bone marrow (BM) c-Kit(+)/Sca-I(+) lineage-negative mononuclear cells (KSL) were examined in T2D mice, db/db mice and KKA^y mice, using EPC colony-forming assay (EPC-CFA).ResultsT2D mice had fewer BM stem/progenitor cells, and proliferation of KSL was lowest in the BM of db/db mice. In T2D mice, the frequency of large colony-forming units (CFUs) derived from BM-KSL was highly reduced, indicating dysfunction of differentiation into mature EPCs. Only a small number of BM-derived progenitors [CD34(+) KSL cells], which contribute to the supply of EPCs for postnatal neovascularization, was also found. Furthermore, in terms of their plasticity to transdifferentiate into various cell types, BM-KSL exhibited a greater potential to differentiate into granulocyte macrophages (GMs) than into other cell types.ConclusionT2D affected EPC colony formation and differentiation of stem cells to mature EPCs or haematopoietic cells. These data suggest opposing regulatory mechanisms for differentiation into mature EPCs and GMs in T2D mice.     

兔外周血与骨髓源性内皮祖细胞培养鉴定及生物学特性的研究

目的:探索并建立兔内皮祖细胞(EPCs)的体外培养、鉴定方法。方法:采用密度梯度分离法分别从兔外周血和骨髓中分离出单个核细胞,接种于预包被明胶的培养瓶,并应用培养基(EBM-2)诱导培养,诱导分化为EPCs;在倒置显微镜下观察两种源性细胞生长过程;台盼蓝法测定细胞传代成活率;通过绘制生长曲线法、MTT法、DNA周期检测比较两种源性获得的EPCs增殖情况;采用免疫荧光染色观察EPCs相关抗原CD34、CD31、CD133及vWF因子的表达。结果:两种源性EPCs均于培养3～4d完全贴壁,呈克隆样生长,7～9d形成类似成熟血管内皮细胞形态,细胞数量逐渐增多,细胞成活率均为95%。两种源性获得的第2代细胞生长曲线近似"s"形、MTT法显示3～5d细胞增殖较明显,外周血源性EPCs G0-G1期和S+G2+M期所占比例分别为96.48%和3.52%,骨髓源性EPCs G0-G1期和S+G2+M期所占比例分别为97.11%和1.84%。第2代EPCs进行免疫荧光鉴定结果显示:两种源性内皮祖细胞均阳性表达CD34、CD133、vWF因子,CD31弱阳性表达。结论:两种源性的EPCs均可高效获得且在体外稳定培养。与传统的骨髓源性EPCs相比较,从外周血源获得的EPCs是一种可靠、简便的培养方法,为组织工程学提供理想的细胞来源。     

巴曲酶对内皮祖细胞功能的影响及其机制的探讨

目的研究巴曲酶(DF-521)对体外培养下内皮祖细胞(EPCs)的增殖、分化、成血管能力以及NO分泌能力的影响,并探讨其可能的机制。方法从人外周血中提取单个核细胞,用流式细胞术检测细胞表型CD34、CD31、血管内皮生长因子2和血管性假血友病因子(vWF),激光共聚焦显微镜观察细胞经过FITC标记的荆豆凝集素I和DiI标记的乙酰化低密度脂蛋白双染色后的情况,由此鉴定EPCs。实验分为:DF-521的低、中、高剂量干预组和对照组。检测各组EPCs的CD31和vWF表达,观察EPCs在基质胶上的成管情况以及测定培养液中NO的浓度。透射电子显微镜鉴定分化后的细胞。结果低、中、高剂量干预组EPCs的数量、CD31、vWF表达及NO浓度均明显高于对照组(P<0.05),而且这些效应随DF-521浓度升高而增加(P<0.05)。高剂量干预组EPCs形成条梭状和管腔样结构。电子显微镜观察到怀布尔-帕拉德小体。结论体外培养务件下.DF-521促进EPCs的增殖和成血管功能,并诱导其向内皮细胞分化,改善分泌NO的能力。DF-521的这些作用可能与内皮型一氧化氮合酶有关。     

外周血内皮祖细胞磁探针标记及体外磁共振成像的实验研究

目的应用纳米磁探针三氧化二铁（Fe2O3）-多聚赖氨酸（PLL）复合物体外标记兔外周血内皮祖细胞（EPCs）,磁共振（MR）对标记细胞成像。方法合成Fe2O3-PLL复合物。分离兔外周血单个核细胞,贴壁法筛选出EPCs,传代培养,Fe2O3-PLL标记祖细胞,普鲁士蓝染色、电子显微镜显示细胞内铁,四氮噻唑蓝（MTT）比色试验评价不同浓度Fe2O3-PLL标记EPCs后对细胞生长状况的影响,流式细胞分析检测标记、未标记细胞的细胞周期、细胞凋亡,应用MR的不同序列进行细胞群成像。结果普鲁士蓝染色、电镜观察均可见铁颗粒位于细胞质内,标记率接近100％,MTT比色试验示10μg／ml至200μg／ml7个铁浓度组,Fe2O3-PLL标记后细胞的光吸收值与未标记者比较,差异无统计学意义,流式细胞分析结果显示Fe2O3-PLL标记后细胞周期、细胞凋亡与未标记细胞间差异无统计学意义。磁共振成像（MRI）显示标记Fe2O3-PLL的细胞群较未标记者信号降低,以T2^＋加权像（FWI）信号强度变化率最大;标记后7d的信号强度变化率均较标记1d者下降。结论Fe2O3-PLL可以有效标记兔外周血EPCs,其对细胞的活力、增殖等生物学特性无明显影响。临床应用型1．5TMR可在体外进行标记细胞群成像,间接反映于细胞的数量和分裂增殖状态。     

颈动脉硬化病人内皮祖细胞增殖和分化能力改变及其临床意义

目的观察颈动脉硬化病人外周血内皮祖细胞(EPCs)增殖和分化能力的改变,探讨其在颈动脉硬化发生发展中的意义。方法选择颈动脉硬化病人和同年龄组正常人各20例,密度梯度离心法从外周血获取单个核细胞,接种在培养板内,培养7d后对贴壁细胞进行鉴定,激光共聚焦显微镜鉴定FITC标记荆豆凝血素-Ⅰ(FITC-UEA-I)和DiI标记的乙酰化低密度脂蛋白(DiI-acLDL)双染色阳性细胞为正在分化的EPCs细胞。四氮唑溴盐比色法(MTT)测定EPCs的增殖能力,流式细胞仪检测细胞表面CD14 ,CD64 和vWF ,测定EPCs向内皮分化能力。结果颈动脉硬化病人外周血EPCs增殖能力较正常对照组显著降低(P<0.05);与正常对照组比较颈动脉硬化组EPCs早期标志物CD14 和CD64 百分比明显升高(P<0.05),而内皮细胞分化的特异性标志物vWF 显著降低(P<0.05)。结论动脉硬化组较正常组外周血EPCs增殖能力和分化为内皮细胞的能力明显减退,血管的再内皮化的过程受损,促进颈动脉硬化的发生发展。     

Endothelial progenitor cells and peripheral neuropathy in subjects with type 2 diabetes mellitus

AimsTo examine for differences in circulating progenitor cells (CPCs) and endothelial progenitor cells (EPCs) in patients with and without diabetic peripheral neuropathy (DPN).MethodsA total of 105 participants were included: 50 patients with type 2 diabetes (T2DM) and DPN, 30 patients with T2DM without DPN and 25 healthy individuals. CPCs and 6 different EPCs phenotypes were assessed with flow cytometry. We also measured plasma levels of vascular endothelial growth factor (VEGF), stromal cell-derived factor 1 (SDF-1), vascular cell adhesion protein-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM) and tumor necrosis factor a (TNFa).ResultsNo difference was observed in the number of CPCs among the 3 groups. Patients with DPN had higher numbers of all 6 EPCs phenotypes when compared with patients without DPN and higher number of 5 EPCs phenotypes when compared with healthy individuals. Plasma VEFG, VCAM-1, ICAM-1 and TNFa levels did not differ among the 3 groups. Patients with DPN had lower SDF-1 levels in comparison with healthy individuals.ConclusionCirculating EPCs are increased while SDF-1 levels are decreased in the presence of DPN. Our findings suggest that DPN may be associated with impaired trafficking of EPCs and impaired EPCs homing to the injured endothelium.     

Statin therapy in patients with coronary artery disease improves the impaired endothelial progenitor cell differentiation into cardiomyogenic cells

Human endothelial progenitor cells (EPCs) can differentiate into cardiomyogenic cells in vitro. We tested the effects of statin therapy on the differentiation rate of EPCs from patients with coronary artery disease (CAD), who may benefit from autologous cell therapy.EPCs from 3 age-matched groups were tested: No CAD (n = 13), CAD patients with (n = 10) or without (n = 16) statin therapy. From 4 CAD patients, EPCs were tested before and after 4 weeks of therapy with 20 mg atorvastatin. After 6 days of co-culture with rat neonatal cardiomyocytes, EPC differentiation was quantified by immunostaining for -sarcomeric actinin flow cytometry analysis. After 6 days of co-culture, the percentage of -sarcomeric actinin–positive EPCs was significantly (p = 0.014) higher in EPCs from adults without CAD (8.07% ± 1.48% of EPCs) compared to EPCs from CAD patients without statin (3.56% ± 0.72%). Importantly, patients with statin therapy revealed significantly higher numbers of -sarcomeric actinin-positive EPCs (6.36% ± 0.69%, p = 0.01) compared to CAD patients without statin. In addition, statin therapy resulted in a significant (p = 0.017) increase of EPC differentiation in all 4 CAD patients investigated before and 4 weeks after statin therapy. The survival of EPCs did not differ between the different groups suggesting that the regulation of EPC differentiation is not secondary to altered EPC survival. In vitro, EPC treatment with 0.1 µM atorvastatin did not affect EPC differentiation (116.15% ± 49.11% of control).EPCs from patients with CAD display impaired differentiation into cardiomyogenic cells. This defect can be improved by in vivo, statin therapy.     

肝细胞生长因子对冠心病患者内皮祖细胞功能的影响

目的观察肝细胞生长因子(HGF)对体外培养冠心病患者外周血内皮祖细胞(EPCs)生物学功能的影响,为HGF在冠心病治疗方面的应用提供研究基础。方法选择冠心病患者(冠心病组)和非冠心病患者(对照组)各15例,每组再随机分为重组人HGF(rhHGF)干预组和非rhHGF干预组,ELISA法检测血浆中HGF水平。流式细胞仪检测EPCs数量,并体外选择培养EPCs,检测rhHGF对EPCs增殖、迁移和黏附能力的影响。结果与对照组比较,冠心痛组患者外周血EPCs数量明显减少,血浆HGF含量明显升高(P0.01);EPCs增殖、黏附和迁移能力明显下降(P0.05,P0.01)。在冠心病组,与非rhHGF干预组比较,rhHGF干预组能明显促进冠心病患者FPCs增殖、黏附和迁移(P0.05,P0.01);在对照组,与非rhHGF干预组比较,rhHGF干预组仅促进对照组患者EPCs增殖,对黏附和迁移虽有促进作用,但差异无统计学意义(P0.05)。结论 HGF可增强冠心病患者EPCs的各项生物学功能,有望将HGF刺激EPCs的生物学活性的作用应用于冠心病的治疗。