中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2015年
15期
4214-4216
,共3页
毛文文%尹列芬%田伟盟%陈国强%周宁%申政磊
毛文文%尹列芬%田偉盟%陳國彊%週寧%申政磊
모문문%윤렬분%전위맹%진국강%주저%신정뢰
2型糖尿病%内皮祖细胞%流式细胞仪
2型糖尿病%內皮祖細胞%流式細胞儀
2형당뇨병%내피조세포%류식세포의
T2DM%EPCs%FCM
目的:观察老年2型糖尿病(T2DM)患者体内内皮祖细胞(EPCs)的功能(以黏附细胞数表示为TNE-A)及其数量(以外周血计数表示为TNE),探讨其在老年T2DM发生发展中的作用。方法选择老年T2DM患者30例和老年正常对照10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7 d后对贴壁细胞进行测定;流式细胞仪鉴定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)双阳性细胞为正常分化的EPCs;胰蛋白酶消化后计数贴壁细胞观察TNE-A计数。同时采用流式细胞仪测定外周血 TNE计数。结果①老年T2DM患者EPCs的TNE-A较正常对照组显著减少,并且血管病变组间也有差异(t=2.185、2.099;P<0.05)。外周血TNE较正常对照组减低(t=2.179; P<0.05),但血管病变各组间无差异(t=1.857; P>0.05)。②随血糖及糖化血红蛋白(HbA1c)升高,T2DM老年患者 TNE-A以及 TNE计数逐渐降低( t=2.872、2.855、2.985、2.861;P<0.01),组间有统计学差异( t=2.122、2.103、2.105、2.175;P<0.05)。③Spearman 相关分析显示, TNE-A水平与低密度脂蛋白( LDL)、舒张压( SBP)、2 h 餐后血糖(2 h PBG)、HbA1c 呈负相关( r分别为-0.40、-0.39、-0.21、-0.24,P<0.01或<0.05)。而外周血TNE与空腹血糖(FBG)、HbA1c呈负相关(r分别为-0.231、-0.267,P<0.05)。④以T2DM 为整体,有血管病变为因变量(有=1,无=0),以年龄等危险因素为自变量,进行Logistic回归分析,SBP、TNE-A进入回归方程。结论 T2DM老年患者EPCs的黏附功能明显受损,与其血管病变关系较大;而外周血EPCs 数目与血管病变关系较小,EPCs生物学功能仍需进一步研究。
目的:觀察老年2型糖尿病(T2DM)患者體內內皮祖細胞(EPCs)的功能(以黏附細胞數錶示為TNE-A)及其數量(以外週血計數錶示為TNE),探討其在老年T2DM髮生髮展中的作用。方法選擇老年T2DM患者30例和老年正常對照10例,密度梯度離心法從外週血穫取單箇覈細胞,接種在培養闆內,培養7 d後對貼壁細胞進行測定;流式細胞儀鑒定FITC標記荊豆凝血素Ⅰ( FITC-UEA-I)和 DiI標記的乙酰化低密度脂蛋白( DiI-acLDL)雙暘性細胞為正常分化的EPCs;胰蛋白酶消化後計數貼壁細胞觀察TNE-A計數。同時採用流式細胞儀測定外週血 TNE計數。結果①老年T2DM患者EPCs的TNE-A較正常對照組顯著減少,併且血管病變組間也有差異(t=2.185、2.099;P<0.05)。外週血TNE較正常對照組減低(t=2.179; P<0.05),但血管病變各組間無差異(t=1.857; P>0.05)。②隨血糖及糖化血紅蛋白(HbA1c)升高,T2DM老年患者 TNE-A以及 TNE計數逐漸降低( t=2.872、2.855、2.985、2.861;P<0.01),組間有統計學差異( t=2.122、2.103、2.105、2.175;P<0.05)。③Spearman 相關分析顯示, TNE-A水平與低密度脂蛋白( LDL)、舒張壓( SBP)、2 h 餐後血糖(2 h PBG)、HbA1c 呈負相關( r分彆為-0.40、-0.39、-0.21、-0.24,P<0.01或<0.05)。而外週血TNE與空腹血糖(FBG)、HbA1c呈負相關(r分彆為-0.231、-0.267,P<0.05)。④以T2DM 為整體,有血管病變為因變量(有=1,無=0),以年齡等危險因素為自變量,進行Logistic迴歸分析,SBP、TNE-A進入迴歸方程。結論 T2DM老年患者EPCs的黏附功能明顯受損,與其血管病變關繫較大;而外週血EPCs 數目與血管病變關繫較小,EPCs生物學功能仍需進一步研究。
목적:관찰노년2형당뇨병(T2DM)환자체내내피조세포(EPCs)적공능(이점부세포수표시위TNE-A)급기수량(이외주혈계수표시위TNE),탐토기재노년T2DM발생발전중적작용。방법선택노년T2DM환자30례화노년정상대조10례,밀도제도리심법종외주혈획취단개핵세포,접충재배양판내,배양7 d후대첩벽세포진행측정;류식세포의감정FITC표기형두응혈소Ⅰ( FITC-UEA-I)화 DiI표기적을선화저밀도지단백( DiI-acLDL)쌍양성세포위정상분화적EPCs;이단백매소화후계수첩벽세포관찰TNE-A계수。동시채용류식세포의측정외주혈 TNE계수。결과①노년T2DM환자EPCs적TNE-A교정상대조조현저감소,병차혈관병변조간야유차이(t=2.185、2.099;P<0.05)。외주혈TNE교정상대조조감저(t=2.179; P<0.05),단혈관병변각조간무차이(t=1.857; P>0.05)。②수혈당급당화혈홍단백(HbA1c)승고,T2DM노년환자 TNE-A이급 TNE계수축점강저( t=2.872、2.855、2.985、2.861;P<0.01),조간유통계학차이( t=2.122、2.103、2.105、2.175;P<0.05)。③Spearman 상관분석현시, TNE-A수평여저밀도지단백( LDL)、서장압( SBP)、2 h 찬후혈당(2 h PBG)、HbA1c 정부상관( r분별위-0.40、-0.39、-0.21、-0.24,P<0.01혹<0.05)。이외주혈TNE여공복혈당(FBG)、HbA1c정부상관(r분별위-0.231、-0.267,P<0.05)。④이T2DM 위정체,유혈관병변위인변량(유=1,무=0),이년령등위험인소위자변량,진행Logistic회귀분석,SBP、TNE-A진입회귀방정。결론 T2DM노년환자EPCs적점부공능명현수손,여기혈관병변관계교대;이외주혈EPCs 수목여혈관병변관계교소,EPCs생물학공능잉수진일보연구。
Objective To investigate the clinical significance of endothelial progenitor cells ( EPCs ) from the older type 2 diabetes mellium(T2DM)patients by the mumbles of EPCs in peripheral blood (TNE)and the adherent mumbles of EPCs cells (TNE-A).Methods EPCs isolated from human peripheral blood of the older T 2DM patient(n=30)and age matched control subjects (n=10).Cytochemical analy-sis was conducted after 7 days culture .EPCs were characterized as Dil-acLDL/FITC-UEA-1 double positive cell detected by FCM .EPCs ad-hesion assay was performed by replacing those on fibronectin-coated dishes .Then TNE-A was counted .TNE in peripheral blood wass detected by FCM.Results TNE-A was significantly impaired in older T2DM group compared with control group (t=2.185,2.099;P<0.05).TNE was deceased in older T2DM patient(t=2.179,P<0.05).TNE-A and TNE were decreased significantly (t=2.872,2.855,2.985,2.861;P<0.01)than those of control group and were also different with the increase of the glucose and HbAlc (P<0.05).There were negative corre-lation between TNE-A and LDL,SBP,2hPBG,HbAlc and too negative correlation between TNE and FBG ,HbAlc(P<0.05 )by Spearman rel-ative analysis.The SBP and TNE-A were valuable by Logistic regressive analysis .Conclusions These findings suggest adhesion function of EPCs may be play an important role in the development of DM .EPCs dysfunction need be further investigated .